1,720,984 research outputs found
Prognostic and pathophysiological roles of circulating dipeptidyl peptidase 3 during circulatory failure
No full textIntroduction : L'insuffisance circulatoire est une cause fréquente d'admission en réanimation, associée à une mortalité importante. Des travaux antérieurs ont démontré l'association entre une concentration de dipeptidyl peptidase 3 circulante (cDPP3) élevée et le pronostic à court terme des patients en insuffisance circulatoire. Nous avons fait l'hypothèse que cDPP3 jouait un rôle pathologique dans la genèse et/ou l'entretien de l'insuffisance circulatoire via son activité de clivage de peptides bioactifs, tels que les angiotensines et les enképhalines. Méthodes : Deux approches ont été utilisées : 1. Sur le plan clinique, l'association entre cDPP3 et le pronostic a été analysée dans des populations de patients souffrant d'insuffisance circulatoire. 2. Sur le plan physiopathologique, les perturbations de l'hémodynamique systémique et rénale induites par cDPP3 ont été investiguées chez la souris. La relation entre les perturbations observées et la modulation du système rénine-angiotensine-aldostérone a été examinée. Résultats : L'analyse des cohortes de patients a permis de confirmer l'association entre cDPP3 et le pronostic à court terme de l'insuffisance circulatoire. Dans la cohorte FROG-ICU, une association similaire entre concentration élevée de cDPP3 à l'inclusion et mortalité à J28 a été observée au cours du choc septique, cardiogénique, ou hémorragique. Dans la cohorte issue de l'essai ACCOST-HH, une concentration élevée de cDPP3 à l'inclusion était également associée à la mortalité à J30, à la durée du support cardiovasculaire ainsi qu'au recours à l'épuration extra-rénale ou à la ventilation mécanique invasive. Les patients chez qui la concentration de cDPP3 restait élevée à H72 avaient le plus mauvais pronostic. En comparaison, les patients ayant une concentration initialement haute mais décroissante de cDPP3 avaient une mortalité significativement réduite, comparable à celle des patients chez qui cDPP3 restait bas. Les patients dont la concentration de cDPP3 restait basse ou s'abaissait à H72 nécessitaient moins de supports d'organes. Chez la souris, l'administration de DPP3 purifié est associée à une augmentation significative du débit sanguin rénal alors que la pression artérielle n'est que peu affectée. L'administration de DPP3 était associée à une diminution significative des concentrations circulantes d'angiotensine II, III et IV en comparaison au contrôle. Une expérience de prétraitement par le valsartan a confirmé que l'effet rénovasculaire de DPP3 était secondaire à la diminution de la stimulation d'AT1R. L'administration de DPP3 était associée à une augmentation des concentrations circulantes de catécholamines endogènes. Une expérience de blocage adrénergique par le labétalol a démontré que ce relargage de catécholamines endogènes expliquait le maintien de la pression artérielle après administration de DPP3. Conclusion : Ces résultats confirment la valeur pronostique de cDPP3 et confortent l'hypothèse d'un rôle pathologique de cDPP3 au cours de l'insuffisance circulatoire, via son activité de clivage des angiotensines. L'effet rénovasculaire suggère également l'implication de cDPP3 dans la genèse de la dysfonction rénale associée à l'insuffisance circulatoire. L'inhibition de cDPP3 pourrait ainsi constituer une stratégie thérapeutique au cours de l'insuffisance circulatoire et devra faire l'objet d'investigations complémentaires.Introduction: Circulatory failure is a frequent cause of admission to the intensive care unit and is associated with significant mortality. Previous research has demonstrated the association between elevated circulating dipeptidyl peptidase 3 (cDPP3) concentration and the short-term prognosis of patients with circulatory failure We hypothesized that cDPP3 plays a pathological role in the development and/or maintenance of circulatory failure through its ability to cleave bioactive peptides such as angiotensins or enkephalins. Methods: Two approaches were used: 1. On a clinical level, the association between cDPP3 and prognosis was analyzed in circulatory failure cohorts. 2. On a pathophysiological level, the hemodynamics changes induced by DPP3 in mice and the relation between the observed effects and renin-angiotensin system modulation were investigated. Results: Analyses of patient cohorts confirmed the association between cDPP3 and short-term prognosis in circulatory insufficiency. In the FROG-ICU cohort, a similar association between elevated cDPP3 concentration at inclusion and 28-day mortality was observed in septic, cardiogenic, or hemorrhagic shock. In the ACCOST-HH trial cohort, a high cDPP3 concentration at inclusion was also associated with 30-day mortality, duration of cardiovascular support, and the need for renal replacement therapy or invasive mechanical ventilation. Patients with persistently high cDPP3 concentrations at H72 had the poorest prognosis. In contrast, patients with initially high but decreasing cDPP3 concentrations had significantly reduced mortality, comparable to those with persistently low cDPP3 concentration. Patients with persistently low or decreasing cDPP3 levels at H72 required less organ support. In mice, administration of purified DPP3 was associated with a significant increase in renal blood flow, while blood pressure was minimally affected. DPP3 administration was associated with a significant decrease in circulating concentrations of angiotensin II, III, and IV, compared to control. A pretreatment experiment with valsartan confirmed that the renovascular effect of DPP3 was secondary to reduced AT1R stimulation. DPP3 administration was associated with increased circulating endogenous catecholamines. Adrenergic blockade by labetalol demonstrated that DPP3-induced release of endogenous catecholamines is responsible for blood pressure maintenance. Conclusion: These results confirm the prognostic value of cDPP3 and support the hypothesis of a pathological role for cDPP3 in circulatory failure through its angiotensin-cleaving activity. The renovascular effect observed also suggests the involvement of cDPP3 in the development of circulatory failure-associated acute kidney injury. Inhibition of cDPP3 may thus represent a therapeutic strategy and warrants further investigation
Detecting subclinical anthracycline therapy related cardiac dysfunction in low income country (SATRACD study)
Full text linkIntroduction: Anthracycline therapy-related cardiac dysfunction (ATRCD) is the most common chemotherapy-induced cardiovascular toxicity. It begins with subclinical myocardial cell injury that can be detected using speckle tracking echocardiography (STE), together with Troponin-I. Limited availability of STE in Uganda posts challenges in detecting subclinical ATRCD. Anthracycline can also affect cancer survivors' cardiovascular health through altering patients' lipid homoeostasis. This PhD project aims to describe the incidence and predictors of subclinical ATRCD, assess the accuracy of simple echocardiographic parameters on detecting subclinical ATRCD and investigate the lipoprotein subfractions change after anthracycline therapy. Methods and results: Two hundred seven cancer patients who were scheduled for anthracycline based chemotherapy were recruited and followed up to 6 months after ending chemotherapy. Patients' clinical characteristics, laboratory tests, electrocardiogram and echocardiographic data were collected at the baseline and at each follow up visits. Among the 207 patients, 178 (86.0%) were female, with a median age of 42 years. The cumulative incidence of subclinical and clinical ATRCD were 35.0% and 8.8% respectively at the 6 months after ending the therapy. No factor was found to predict subclinical ATRCD in multivariable model. The development of clinical ATRCD associated with HIV infection and development of subclinical ATRCD at the end of anthracycline therapy. The reduction of mitral annular plane systolic excursion (ΔMAPSE) ≥ 2mm or reduction of mitral annular peak systolic velocity (Δ S') ≥ 0.5cm/s from the baseline defined subclinical ATRCD with fairly good accuracy. Very low density lipoprotein subfraction increased and mean low density lipoprotein particle size decreased following anthracycline therapy. Conclusion: There is high incidence of subclinical ATRCD in Uganda cancer patients. Cardiac surveillance at baseline and ending of anthracycline therapy is essential to identify subclinical ATRCD patients who are at high risk of developing clinical ATRCD, particular in HIV positive patients. The conventional echocardiographic parameters ΔMAPSE and ΔS' may be used to screen subclinical ATRCD in resource limited settings. Anthracycline changes lipoprotein subfraction to more atherogenic pattern. Further studies are needed to explore more on its role on lipid metabolism
Source et mécanisme de libération de la Dipeptidyl peptidase 3 (DPP3) dans les situations pathologiques
No full textIntroduction : La Dipeptidyl peptidase 3 (DPP3) est une métallopeptidase intracellulaire, également détectée dans la circulation (cDPP3) de sujets sains et de patients en état critique. Elle a été identifiée comme un biomarqueur pronostique et une cible thérapeutique potentielle de l'insuffisance circulatoire. Notre premier objectif était de valider la valeur pronostique de cDPP3 dans l'hémorragie du post-partum sévère (HPPs). La source et les mécanismes de libération de DPP3 dans la circulation demeurent inconnus. Étant donné que des concentrations élevées de cDPP3 sont souvent associées à une inflammation systémique marquée, nous formulons l'hypothèse que les cellules de la moelle osseuse (CMO) pourraient constituer une source potentielle de cDPP3. Méthodes : Sur l'axe clinique, l'association entre les niveaux de cDPP3 et la survenue d'événements cardiovasculaires (ECVs) a été évaluée dans les jours suivant la HPPs dans la cohorte HELP-MOM. Sur l'axe préclinique, un modèle murin de dysfonction cardiaque induite par l'isoprotérénol (ISO) a été utilisé. L'expression protéique de DPP3 dans les CMO et son activité enzymatique dans le plasma et le surnageant de moelle osseuse (SN MO) ont été mesurées. De plus, un modèle d'irradiation corporelle totale suivie d'une greffe de moelle osseuse hétérologue (GMO) entre les souris WT et DPP3-KO a été appliqué, suivi par l'injection d'ISO ou de PBS aux souris chimériques, six semaines après la GMO. Afin d'investiguer le mécanisme de libération, des vésicules extracellulaires (VEs) de grande (gVEs) et de petites (pVEs) taille ont été isolées à partir du SN MO des souris par ultracentrifugation. Résultats : L'analyse de la cohorte de patientes atteintes de HPPs a montré une association significative, même après ajustement pour les variables confondantes, entre la concentration de cDPP3 et la survenue des ECVs (Odds ratio OR=3.41, p=0.025). Dans le modèle ISO, l'expression de DPP3 était significativement augmentée dans les CMO des souris ISO par rapport aux contrôles (1.9X, p<0.05). De plus, l'activité de cDPP3 était significativement augmentée à la fois dans le SN MO (1.3X, p<0.05) et dans le plasma (1.9X, p<0.05) des souris ISO par rapport aux contrôles. Quatre semaines post-GMO, les souris KO greffées avec de la moelle osseuse WT (KO^ MO WT) avaient une activité de cDPP3 équivalente à 44 % de celle des souris WT, indiquant que les CMO représentent une source majeure de cDPP3 dans des conditions physiologiques. De plus, l'activité de cDPP3 chez les souris KO^ MO WT traitées par ISO était significativement augmentée par rapport aux souris KO^ MO WT traitées par PBS (2.2X, p<0.01), démontrant que les CMO sont, au moins en partie, responsables de l'augmentation de cDPP3 observée lors de l'induction d'une dysfonction cardiaque. Les souris KO^ MO WT présentaient une activité de DPP3 dans l'ensemble des organes, indiquant que les CMO pourraient jouer un rôle dans le transport de DPP3 vers les tissus. Dans le modèle ISO, la proportion moyenne de l'activité de DPP3 associée aux VEs dérivées du SN MO par rapport à l'activité totale dans le SN MO était d'environ 11 % pour les gVEs et de 8 % pour les petites pVEs chez les souris témoins, sans différence d'activité par rapport aux souris traitées à l'ISO. En outre, une activité de DPP3 a été détectée dans les VEs isolées à partir du SN MO des souris KO^ MO WT, confirmant ainsi l'origine médullaire de ces vésicules contenant DPP3. Conclusion : Nos résultats confirment la valeur pronostique de cDPP3 et soutiennent l'hypothèse que les CMO constituent une source majeure de la libération de DPP3 dans la circulation et dans les tissus, aussi bien dans des conditions physiologiques que lors de stress cardiaque aigu, et que les VEs sont impliquées dans ce mécanisme de libération.Introduction: Dipeptidyl peptidase 3 (DPP3) is an intracellular metallopeptidase but has also been detected in the circulation (cDPP3) of healthy individuals and critically-ill patients. It has recently emerged as a prognostic biomarker and a promising therapeutic target in circulatory failure. We first aimed to validate the prognosis value of cDPP3 in a cohort of severe postpartum haemorrhage (sPPH). The source and mechanism of DPP3 release into the circulation are not known yet. Considering that elevated levels of cDPP3 were often associated with high levels of systemic inflammation, we hypothesis that Bone Marrow Cells (BMCs) might be a possible source of cDPP3. Methods: In the clinical axis, HELP-MOM cohort of patients with sPPH was studied, and the association between cDPP3 levels and occurrence of cardiovascular events (CVEs) was evaluated in the days following sPPH. In the preclinical axis, an isoproterenol (ISO) induced acute cardiac dysfunction mouse model was used. DPP3 protein expression in BMCs was evaluated by western blot and its enzymatic activity was measured in the plasma and bone marrow supernatant (BM SN). Furthermore, a model of total body irradiation followed by a heterologous bone marrow transplantation (BMT) between WT and DPP3-KO mice was applied, followed by ISO or PBS injection in the resulting chimeric mice at 6 weeks post-BMT. To investigate DPP3 release mechanism, large (lEVs) and small (sEVs) Extracellular Vesicles (EVs) were isolated from mice BM SN by ultracentrifugation and DPP3 activity in these EVs was evaluated as well. Results: The analysis of HELP-MOM cohort of sPPH patients demonstrated a significant association between cDPP3 concentration and occurrence of CVEs which remained significant after adjusting for confounding variables (Odds ratio OR=3.41, p=0.025). In vivo, DPP3 protein expression was increased in BMCs from ISO treated animal versus controls (1.9X, p<0.05). Furthermore, cDPP3 activity was significantly increased in both BM SN (1.3X, p<0.05) and plasma (1.9X, p<0.05) of ISO mice compared to controls. Results from BMT model demonstrate that, KO mice transplanted with WT bone marrow (KO^ BM WT mice), at 4 weeks post-BMT, had a cDPP3 activity equivalent to 44% of cDPP3 activity in WT mice at baseline, reflecting that BMCs represent a major source of cDPP3 in physiological conditions. Furthermore, cDPP3 activity in ISO-treated KO^ BM WT was significantly increased compared to PBS-treated KO^ BM WT (2.2X, p<0.01), demonstrating that BMCs are responsible, at least partially, for the increase in cDPP3 witnessed upon induction of cardiac dysfunction. KO^ BM WT mice showed an activity of DPP3 in all organs reflecting that BMCs might play a role in bringing DPP3 into the tissues. In ISO model, the mean percentage of DPP3 activity in BM SN-derived EVs to its total activity in BM SN was around 11 % in lEVs and 8% in sEVs in control mice with no significant difference in activity between Ctrl and ISO mice. Furthermore, DPP3 activity was detected in EVs from BM SN of KO^ BM WT mice, confirming the BM origin of these vesicles containing DPP3. Conclusion: Our results confirm the prognostic value of cDPP3 and support the hypothesis that BMCs represent a major source of cDPP3 release into the circulation and injured cardiac tissue in both physiological and acute cardiac stress conditions and that EVs are implicated in this release
Characterisation of cardiac remodeling associated with pregnancy: providing insights to peripartum cardiomyopathy
Full text linkIntroduction: Maternal cardiovascular changes that occur in pregnant women are usually well tolerated by most women experiencing an uncomplicated pregnancy and are reversable postpartum. However, pregnancy can induce adverse cardiac events in previously healthy women without any known cardiovascular disease. Understanding of the maternal cardiovascular adaptation during healthy pregnancy is important to identify deviations from regular patterns caused by pathological conditions. The main objective of this study was to explore the functional, structural and molecular cardiovascular changes that are involved in healthy pregnancy with the goal to delineate possible mechanisms involved in the lack of reverse cardiovascular remodeling observed in peripartum cardiomyopathy (PPCM). Methods: Cardiovascular functional, morphological and molecular changes during pregnancy and postpartum were assessed in pregnant wild type mice (C57/BL6) and healthy women. An invitro model of cardiac hypertrophy was then used to explore the involvement of pregnancy hormones in the regulation of cardiac hypertrophy. Finally, we assessed the circulatory level of growth differentiation 15 (GDF-15) in PPCM patients and matched healthy controls. Results: Cardiac structural, functional and morphological changes were observed in mice and all the parameters were resolved postpartum. Strikingly, volume load, cardiac hypertrophy and fibrosis were sustained for a longer period postpartum than previously reported. Proteomics profiling confirmed the prolongation of cardiac hypertrophy in the postpartum and the involvement of the ubiquitin proteasome system (UPS) in the reverse remodeling of cardiac changes that occur during pregnancy. We also identified a set of transcription factors that regulates the protein expression in the postpartum. Left ventricular systolic function was significantly reduced in late pregnancy in humans. Finally, the serum level of GDF-15 was significantly lower in PPCM patients compared to healthy controls Conclusion: We conclude that pregnancy induces cardiac stress which is sustained in the postpartum period. The heart remodels and adapts to meet the demand by both the mother and the fetus. Cardiac changes that occur during pregnancy are strictly regulated and reversed postpartum. However, the postpartum period is a period of intense cardiac stress and activity which requires monitoring for any deviation that may lead to pathological conditions
Targeting heart rate as a novel therapeutic approach in acute heart failure
No full textBackground and hypothesis: Standard pharmacological treatment for heart failure improves cardiac remodelling and survival in the setting of chronic heart failure, but is suboptimal in cases of acute heart failure (AHF). Peripartum cardiomyopathy (PPCM), de-novo hypotension (often due to haemorrhagic shock), and Takotsubo cardiomyopathy (TC) are conditions which have acute onset of heart failure, and often present with high mortality rates. In patients treated for these pathologies, a variation in the heart rate is observed and could potentially be used as a target to improve the treatment of AHF. We therefore questioned whether the use of a sinoatrial node inhibitor (ivabradine) to modulate heart rate may improve outcomes in AHF. Objectives and methods: Our objectives were 3-fold: (1) to explore the effect of a standard treatment strategy on heart rate in a South African cohort of PPCM patients after 6 and 12 months follow-up. (2) To explore the effect of ivabradine, a sinoatrial node inhibitor in an established signal transducer and activator of transcription 3 (STAT3) knockout mouse model of PPCM (with 3 consecutive pregnancies). Mice were fed ivabradine for 30 days (10mg/kg/day in drinking water), following the 3rd weaning. Trans-thoracic echocardiograms (TTE) were done at the end of the 3rd weaning, and after 30 days of treatment with ivabradine. Hearts were harvested after the second TTE for histology staining and messenger ribonucleic acid (mRNA) quantitation of transcripts involved in heart failure. (3) To explore the role of the sinoatrial node inhibitor in an ex-vivo model of de-novo AHF due to hypotension, and a newly developed ex-vivo model of TC. In the AHF model, hearts were stabilised before administering Ivabradine (3μM) in a buffer containing high free fatty-acids at a low pressure (to mimic hypotension/ haemorrhage shock conditions). A pressure- sensing balloon in the left ventricle measured heart rate, diastolic and systolic pressure, left ventricular developed pressure, rate pressure products and functional recovery. In the TC model, hearts were stabilised, then given a buffer with high free fatty-acid content and 10 times a physiological dose of adrenaline to mimic the adrenergic response seen in TC. Thereafter, hearts were restored to stabilisation pressure and substrate for recovery. Results: (1) Clinical outcomes indicated that patients on maximum standard therapy improved symptomatically and on the New York Heart Association scale. However, heart rates of PPCM patients remained elevated after 6 months of treatment. (2) In PPCM mice, a treatment with ivabradine was associated with reduced fibrotic infiltration in cardiac tissue and with a decrease in levels of atrial natriuretic peptide and Fibronectin mRNAs. (3) Both hypotensive AHF and TC models showed a tendency toward better cardiac function with ivabradine at the end of the acute phases. This advantage was lost after withdrawal of ivabradine during recovery. Conclusion: In South African women with PPCM treated with standard therapy, heart rate remains elevated, therefore suggesting that these women may benefit from the use of ivabradine as an additional therapy, particularly in patients who may be intolerant to β-blockers. The long-term use of ivabradine in the setting of cardiac dysfunction appears to have beneficial effects on remodelling, as treatment with ivabradine in our mouse PPCM model showed reduced cardiac fibrosis. The ex-vivo models of hypotensive AHF and TC both showed benefit in reducing heart rate during the acute phases, and hold the potential of being an intervention therapy to improve the outcome in patients who are brought to hospital while still in the acute phase
Effets de l'hyperaldostéronisme cardiaque sur les mécanismes impliqués dans le développement de l'hypertrophie et la fibrose dans le cœur hypertendu
No full textL hypertension artérielle (HTA) est l une des causes de morbidité cardiovasculaire. Le rôle que joue l aldostérone cardiaque dans les mécanismes impliqués dans le développement de l hypertrophie et de la fibrose cardiaques induite par l HTA, demeure encore mal compris. Pour ce faire, nous crée une souris doublement transgénique issue d un croisement entre un mâle AS (qui surexprime l aldostérone synthase dans le cardiomyocyte, avec une femelle RenTgKC (qui surexprime la rénine dans le foie entraînant une augmentation progressive de l angiotensine II (Ang II) plasmatique, un excellent modèle d HTA). La souris double-transgénique AS-Ren va nous permettre d étudier les effets de l aldostérone cardiaque lors du remodelage cardiaque induit par une HTA, ainsi que les intéractions entre l aldostérone et l Ang II. Avec un même niveau de pression artérielle que les souris Ren, les souris AS-Ren présentent une l'hypertrophie et une fibrose cardiaques plus importante que celles induites par l HTA seule. Nos résultats démontrent pour la première fois que l aldostérone via son récepteur minéralocorticoïde (RM) inhibe l induction par l HTA de l ANP et de la ßMyHC via des mécanismes impliquant respectivement la voie cAMP-CREB et les miR-208. L inhibition de l ANP est responsable in fine de l aggravation de l hypertrophie. Concernant la fibrose, nous démontrons que l'effet profibrosant de l'aldostérone est principalement attribuable à l'inhibition précoce et soutenue des facteurs antifibrotiques (BNP, BMP4) suivie d activation des mécanismes pro-inflammatoires, déséquilibrant la balance entre les facteurs profibrosants et les facteurs antifibrosants. L ensemble de ces résultats permet de mieux comprendre les mécanismes d action de l aldostérone cardiaque, désigne de nouvelles cibles de l aldostérone telles que les peptides natriurétiques et affirme l effet bénéfique de l antagonisme du RM dans le remodelage cardiaque induit par l hypertension artérielleArterial hypertension (AH) is one of the major causes of the transition to heart failure. The role of aldosterone in cardiac mechanisms involved in the development of hypertrophy and cardiac fibrosis in AH remain poorly understood. To do this, we crossed a male AS (transgenic mice that overexpress aldosterone synthase in the cardiomyocyte, which leads to a 2 fold increase of cardiac aldosterone concentration) with a female RenTgKC (transgenic mice that overexpress renin in the liver that which induces a gradual increase in plasma Angiotensine II. These mice represent an excellent model of hypertension). Double-transgenic resulting mouse AS-Ren will thus allow us to study the cardiac effects of aldosterone in cardiac remodeling induced by hypertension, as well as the interactions between aldosterone and angiotensin 2 (Ang II). For the same level of blood pressure than Ren mice, AS-Ren mice have a worsening of hypertrophy and cardiac fibrosis induced by hypertension. Our results show for the first time that aldosterone via the mineralocorticoid receptor (RM) inhibits the induction by hypertension of ANP and ßMyHC expressions via a mechanistic pathway involving the cAMP-CREB and miR-208, respectively. Inhibition of ANP is ultimately responsible for the worsening of hypertrophy. With regard to fibrosis, we demonstrate that the profibrotic effect of aldosterone is mainly due to an early and sustained inhibition of antifibrotic factors (BNP, BMP4) followed by a proinflammatory activation, and thus worsening the imbalance between factors profibrotic and antifibrotic factors. All of these results permit to better understand the mechanisms of action of cardiac aldosterone, designate new aldosterone s targets, such as natriuretic peptides and affirms the beneficial effect of RM antagonism in cardiac remodeling induced by hypertensionPARIS-BIUSJ-Biologie recherche (751052107) / SudocSudocFranceF
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe 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
Full text link“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
Full text linkWe 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
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