Static GPS measurements and elevation model in the vicinity of the EDML deep-drilling site

Interpretation of ice-core records requires accurate knowledge of the past and present surface topography and stress-strain fields. The European Project for Ice Coring in Antarctica (EPICA) drilling site (0.0684° E and 75.0025° S, 2891.7 m) in Dronning Maud Land, Antarctica, is located in the immediate vicinity of a transient and splitting ice divide. A digital elevation model is determined from the combination of kinematic GPS measurements with the GLAS12 data sets from the ICESat satellite. Based on a network of stakes, surveyed with static GPS, the velocity field around the EDML drilling site is calculated. The annual mean velocity magnitude of 12 survey points amounts to 0.74 m/a. Flow directions mainly vary according to their distance from the ice divide. Surface strain rates are determined from a pentagon-shaped stake network with one center point, close to the drilling site. The strain field is characterised by along flow compression, lateral dilatation, and vertical layer thinning.

Sedimentation and mineral analysis on sediment cores from the Lena Delta

Core and outcrop analysis from Lena mouth deposits have been used to reconstruct the Late Quaternary sedimentation history of the Lena Delta. Sediment properties (heavy mineral composition, grain size characteristics, organic carbon content) and age determinations (14C AMS and IR-OSL) are applied to discriminate the main sedimentary units of the three major geomorphic terraces, which form the delta. The development of the terraces is controlled by complex interactions among the following four factors: (1) Channel migration. According to the distribution of 14C and IR-OSL age determinations of Lena mouth sediments, the major river runoff direction shifted from the west during marine isotope stages 5-3 (third terrace deposits) towards the northwest during marine isotope stage 2 and transition to stage 1 (second terrace), to the northeast and east during the Holocene (first terrace deposits). (2) Eustasy. Sea level rise from Last Glacial lowstand to the modern sea level position, reached at 6-5 ka BP, resulted in back-filling and flooding of the palaeovalleys. (3) Neotectonics. The extension of the Arctic Mid-Ocean Ridge into the Laptev Sea shelf acted as a halfgraben, showing dilatation movements with different subsidence rates. From the continent side, differential neotectonics with uplift and transpression in the Siberian coast ridges are active. Both likely have influenced river behavior by providing sites for preservation, with uplift, in particular, allowing accumulation of deposits in the second terrace in the western sector. The actual delta setting comprises only the eastern sector of the Lena Delta. (4) Peat formation. Polygenetic formation of ice-rich peaty sand (''Ice Complex'') was most extensive (7-11 m in thickness) in the southern part of the delta area between 43 and 14 ka BP (third terrace deposits). In recent times, alluvial peat (5-6 m in thickness) is accumulated on top of the deltaic sequences in the eastern sector (first terrace).

Global Scale Impacts

Global scale impacts modify the physical or thermal state of a substantial fraction of a target asteroid. Specific effects include accretion, family formation, reshaping, mixing and layering, shock and frictional heating, fragmentation, material compaction, dilatation, stripping of mantle and crust, and seismic degradation. Deciphering the complicated record of global scale impacts, in asteroids and meteorites, will lead us to understand the original planet-forming process and its resultant populations, and their evolution in time as collisions became faster and fewer. We provide a brief overview of these ideas, and an introduction to models.

Investigación sobre las causas que pudieron originar el hundimiento de la cubierta del tercer depósito del Canal de Isabel II en 1905

En la presente investigación se analiza la causa del hundimiento del cuarto compartimento del Tercer Depósito del Canal de Isabel II el 8 de abril de 1905, uno de los más graves de la historia de la construcción en España: fallecieron 30 personas y quedaron heridas otras 60. El Proyecto y Construcción de esta estructura era de D. José Eugenio Ribera, una de las grandes figuras de la ingeniería civil en nuestro país, cuya carrera pudo haber quedado truncada como consecuencia del siniestro. Dado el tiempo transcurrido desde la ocurrencia de este accidente, la investigación ha partido de la recopilación de la información relativa al Proyecto y a la propia construcción de la estructura, para revisar a continuación la información disponible sobre el hundimiento. De la construcción de la cubierta es interesante destacar la atrevida configuración estructural, cubriéndose una inmensa superficie de 74.000 m2 mediante una sucesión de bóvedas de hormigón armado de tan sólo 5 cm de espesor y un rebajamiento de 1/10 para salvar una luz de 6 m, que apoyaban en pórticos del mismo material, con pilares también muy esbeltos: 0,25 m de lado para 8 m de altura. Y todo ello en una época en la que la tecnología y conocimiento de las estructuras con este "nuevo" material se basaban en buena medida en el desarrollo de patentes. En cuanto a la información sobre el hundimiento, llama la atención en primer lugar la relevancia de los técnicos, peritos y letrados que intervinieron en el juicio y en el procedimiento administrativo posterior, poniéndose de manifiesto la trascendencia que el accidente tuvo en su momento y que, sin embargo, no ha trascendido hasta nuestros días. Ejemplo de ello es el papel de Echegaray -primera figura intelectual de la época- como perito en la defensa de Ribera, de D. Melquiades Álvarez -futuro presidente del Congreso- como abogado defensor, el General Marvá -uno de los máximos exponentes del papel de los ingenieros militares en la introducción del hormigón armado en nuestro país-, que presidiría la Comisión encargada del peritaje por parte del juzgado, o las opiniones de reconocidas personalidades internacionales del "nuevo" material como el Dr. von Emperger o Hennebique. Pero lo más relevante de dicha información es la falta de uniformidad sobre lo que pudo ocasionar el hundimiento: fallos en los materiales, durante la construcción, defectos en el diseño de la estructura, la realización de unas pruebas de carga cuando se concluyó ésta, etc. Pero la que durante el juicio y en los Informes posteriores se impuso como causa del fallo de la estructura fue su dilatación como consecuencia de las altas temperaturas que se produjeron aquella primavera. Y ello a pesar de que el hundimiento ocurrió a las 7 de la mañana... Con base en esta información se ha analizado el comportamiento estructural de la cubierta, permitiendo evaluar el papel que diversos factores pudieron tener en el inicio del hundimiento y en su extensión a toda la superficie construida, concluyéndose así cuáles fueron las causas del siniestro. De los resultados obtenidos se presta especial atención a las enseñanzas que se desprenden de la ocurrencia del hundimiento, enfatizándose en la relevancia de la historia -y en particular de los casos históricos de error- para la formación continua que debe existir en la Ingeniería. En el caso del hundimiento del Tercer Depósito algunas de estas "enseñanzas" son de plena actualidad, tales como la importancia de los detalles constructivos en la "robustez" de la estructuras, el diseño de estructuras "integrales" o la vigilancia del proceso constructivo. Por último, la investigación ha servido para recuperar, una vez más, la figura de D. José Eugenio Ribera, cuyo papel en la introducción del hormigón armado en España fue decisivo. En la obra del Tercer Depósito se arriesgó demasiado, y provocó un desastre que aceleró la transición hacia una nueva etapa en el hormigón estructural al abrigo de un mayor conocimiento científico y de las primeras normativas. También en esta etapa sería protagonista. This dissertation analyses the cause of the collapse of the 4th compartment of the 3th Reservoir of Canal de Isabel II in Madrid. It happened in 1905, on April 8th, being one of the most disastrous accidents occurred in the history of Spanish construction: 30 people died and 60 were injured. The design and construction supervision were carried out by D. José Eugenio Ribera, one of the main figures in Civil Engineering of our country, whose career could have been destroyed as a result of this accident. Since it occurred more than 100 years ago, the investigation started by compiling information about the structure`s design and construction, followed by reviewing the available information about the accident. With regard to the construction, it is interesting to point out its daring structural configuration. It covered a huge area of 74.000 m2 with a series of reinforced concrete vaults with a thickness of not more than 5 cm, a 6 m span and a rise of 1/10th. In turn, these vaults were supported by frames composed of very slender 0,25 m x 0,25 m columns with a height of 8 m. It is noteworthy that this took place in a time when the technology and knowledge about this "new" material was largely based on patents. In relation to the information about the collapse, its significance is shown by the important experts and lawyers that were involved in the trial and the subsequent administrative procedure. For example, Echegaray -the most important intellectual of that time- defended Ribera, Melquiades Álvarez –the future president of the Congress- was his lawyer, and General Marvá -who represented the important role of the military engineers in the introduction of reinforced concrete in our country-, led the Commission that was put in charge by the judge of the root cause analysis. In addition, the matter caught the interest of renowned foreigners like Dr. von Emperger or Hennebique and their opinions had a great influence. Nonetheless, this structural failure is unknown to most of today’s engineers. However, what is most surprising are the different causes that were claimed to lie at the root of the disaster: material defects, construction flaws, errors in the design, load tests performed after the structure was finished, etc. The final cause that was put forth during the trial and in the following reports was attributed to the dilatation of the roof due to the high temperatures that spring, albeit the collapse occurred at 7 AM... Based on this information the structural behaviour of the roof has been analysed, which allowed identifying the causes that could have provoked the initial failure and those that could have led to the global collapse. Lessons have been learned from these results, which points out the relevance of history -and in particular, of examples gone wrong- for the continuous education that should exist in engineering. In the case of the 3th Reservoir some of these lessons are still relevant during the present time, like the importance of detailing in "robustness", the design of "integral" structures or the due consideration of construction methods. Finally, the investigation has revived, once again, the figure of D. José Eugenio Ribera, whose role in the introduction of reinforced concrete in Spain was crucial. With the construction of the 3th Reservoir he took too much risk and caused a disaster that accelerated the transition to a new era in structural concrete based on greater scientific knowledge and the first codes. In this new period he would also play a major role.

Transient cardiac expression of constitutively active Gαq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways

Cardiac hypertrophy and dilatation can result from stimulation of signal transduction pathways mediated by heterotrimeric G proteins, especially Gq, whose α subunit activates phospholipase Cβ (PLCβ). We now report that transient, modest expression of a hemagglutinin (HA) epitope-tagged, constitutively active mutant of the Gq α subunit (HAα*q) in hearts of transgenic mice is sufficient to induce cardiac hypertrophy and dilatation that continue to progress after the initiating stimulus becomes undetectable. At 2 weeks, HAα*q protein is expressed at less than 50% of endogenous αq/11, and the transgenic hearts are essentially normal morphologically. Although HAα*q protein declines at 4 weeks and is undetectable by 10 weeks, the animals develop cardiac hypertrophy and dilatation and die between 8 and 30 weeks in heart failure. As the pathology develops, endogenous αq/11 rises (2.9-fold in atria; 1.8-fold in ventricles). At 2 weeks, basal PLC activity is increased 9- to 10-fold in atria but not ventricles. By 10 weeks, it is elevated in both, presumably because of the rise in endogenous αq/11. We conclude that the pathological changes initiated by early, transient HAα*q expression are maintained in part by compensatory changes in signal transduction and other pathways. Cyclosporin A (CsA) prevents hypertrophy caused by activation of calcineurin [Molkentin, J. D., Lu, J.-R., Antos, C. L., Markham, B., Richardson, J., Robbins, J., Grant, S. R. & Olson, E. N. (1998) Cell 93, 215–228]. Because HAα*q acts upstream of calcineurin, we hypothesized that HAα*q might initiate additional pathways leading to hypertrophy and dilatation. Treating HAα*q mice with CsA diminished some, but not all, aspects of the hypertrophic phenotype, suggesting that multiple pathways are involved.

Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A

Natriuretic peptides, produced in the heart, bind to the natriuretic peptide receptor A (NPRA) and cause vasodilation and natriuresis important in the regulation of blood pressure. We here report that mice lacking a functional Npr1 gene coding for NPRA have elevated blood pressures and hearts exhibiting marked hypertrophy with interstitial fibrosis resembling that seen in human hypertensive heart disease. Echocardiographic evaluation of the mice demonstrated a compensated state of systemic hypertension in which cardiac hypertrophy and dilatation are evident but with no reduction in ventricular performance. Nevertheless, sudden death, with morphologic evidence indicative in some animals of congestive heart failure and in others of aortic dissection, occurred in all 15 male mice lacking Npr1 before 6 months of age, and in one of 16 females in our study. Thus complete absence of NPRA causes hypertension in mice and leads to cardiac hypertrophy and, particularly in males, lethal vascular events similar to those seen in untreated human hypertensive patients.

Lipotoxic heart disease in obese rats: Implications for human obesity

To determine the mechanism of the cardiac dilatation and reduced contractility of obese Zucker Diabetic Fatty rats, myocardial triacylglycerol (TG) was assayed chemically and morphologically. TG was high because of underexpression of fatty acid oxidative enzymes and their transcription factor, peroxisome proliferator-activated receptor-α. Levels of ceramide, a mediator of apoptosis, were 2–3 times those of controls and inducible nitric oxide synthase levels were 4 times greater than normal. Myocardial DNA laddering, an index of apoptosis, reached 20 times the normal level. Troglitazone therapy lowered myocardial TG and ceramide and completely prevented DNA laddering and loss of cardiac function. In this paper, we conclude that cardiac dysfunction in obesity is caused by lipoapoptosis and is prevented by reducing cardiac lipids.

Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice

Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to βadrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein–kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein–kinin system could be involved in the development or progression of cardiovascular diseases.

The Golgi apparatus of spinal cord motor neurons in transgenic mice expressing mutant Cu,Zn superoxide dismutase becomes fragmented in early, preclinical stages of the disease.

Dominant mutations of the SOD1 gene encoding Cu,Zn superoxide dismutase have been found in members of certain families with familial amyotrophic lateral sclerosis (ALS). To better understand the contribution of SOD1 mutations in the pathogenesis of familial ALS, we developed transgenic mice expressing one of the mutations found in familial ALS. These animals display clinical and pathological features closely resembling human ALS. Early changes observed in these animals were intra-axonal and dendritic vacuoles due to dilatation of the endoplasmic reticulum and vacuolar degeneration of mitochondria. We have reported that the Golgi apparatus of spinal cord motor neurons in patients with sporadic ALS is fragmented and atrophic. In this study we show that spinal cord motor neurons of transgenic mice for an SOD1 mutation display a lesion of the Golgi apparatus identical to that found in humans with sporadic ALS. In these mice, the stacks of the cisternae of the fragmented Golgi apparatus are shorter than in the normal organelle, and there is a reduction in Golgi-associated vesicles and adjacent cisternae of the rough endoplasmic reticulum. Furthermore, the fragmentation of the Golgi apparatus occurs in an early, presymptomatic stage and usually precedes the development of the vacuolar changes. Transgenic mice overexpressing the wild-type human superoxide dismutase are normal. In familial ALS, an early lesion of the Golgi apparatus of motor neurons may have adverse functional effects, because newly synthesized proteins destined for fast axoplasmic transport pass through the Golgi apparatus.

cGMP mediates the vascular and platelet actions of nitric oxide: confirmation using an inhibitor of the soluble guanylyl cyclase.

The L-arginine:nitric oxide (NO) pathway is believed to exert many of its physiological effects via stimulation of the soluble guanylyl cyclase (SGC); however, the lack of a selective inhibitor of this enzyme has prevented conclusive demonstration of this mechanism of action. We have found that the compound 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ) inhibits the elevation of cGMP induced by the NO donor S-nitroso-DL-penicillamine in human platelets and rat vascular smooth muscle (IC50 = 10-60 nM and <10 nM, respectively) and that this is accompanied by prevention of the platelet inhibitory and vasodilator actions of NO donors. ODQ also inhibited the antiaggregatory action of NO generated by the platelets but did not affect the action of prostacyclin or that of a cGMP mimetic. In addition, ODQ inhibited the vasodilator actions of endogenously released NO and of NO generated after induction of NO synthase in vascular preparations. It did not, however, affect the increase in vascular smooth muscle cGMP or the dilatation induced by atrial natriuretic factor. ODQ had no effect on NO synthase activity, nor did it react with NO. It did, however, potently (IC50 approximately 10 nM) inhibit the activity of the SGC in cytosol obtained from crude extract of rat aortic smooth muscle. Thus ODQ prevents the actions of NO on platelets and vascular smooth muscle through its potent inhibitory effect on the SGC.

Rastreamento do olhar na avaliação de presença em atividades mediadas por vídeo.

A percepção de presença (PP), evolução do conceito de telepresença, pode ser definida como ilusão perceptiva de não mediação e/ou a percepção ilusória da realidade. O método mais utilizado para a avaliação da PP faz uso de questionários aplicados aos sujeitos, após sua participação numa experiência. Além de não fornecer informações em tempo real esse método sofre muitas interferências advindas tanto dos sujeitos submetidos ao experimento como dos avaliadores dos questionários. Os métodos que poderiam ser mais efetivos para a avaliação da PP, em tempo real, fazem uso de sinais fisiológicos que variam independentemente da vontade dos sujeitos, como batimento cardíaco, eletrocardiograma, eletroencefalograma, resistividade e umidade da pele. Os sinais fisiológicos, no entanto, só variam de forma significativa em situações de estresse, inviabilizando sua utilização em atividades normais, sem estresse. Outra forma de avaliar a PP é utilizar sistemas de rastreamento do olhar. Estudados e desenvolvidos desde o século 19, os sistemas de rastreamento do olhar fornecem um mapeamento do movimento dos olhos. Além de indicar para onde os sujeitos estão olhando, podem também monitorar a dilatação da pupila e as piscadas. Atualmente existem sistemas de rastreamento do olhar comerciais de baixo custo, que apesar de terem menos precisão e frequência que os equipamentos de alto custo são mais práticos e possuem software de plataforma aberta. No futuro serão tão comuns e simples de usar como são hoje as câmeras em dispositivos móveis e computadores, o que viabilizará a aplicação das técnicas e métodos aqui propostos em larga escala, principalmente para monitorar a atenção e envolvimento de atividades mediadas por vídeo. É apresentada uma ferramenta que faz uso do rastreamento do olhar para avaliar a percepção de presença em atividades mediadas por vídeo (com estímulos sonoros). Dois experimentos foram realizados para validar as hipóteses da pesquisa e a ferramenta. Um terceiro experimento foi executado para verificar a capacidade da ferramenta em avaliar a percepção de presença em atividades não estressantes mediadas por vídeo.

Automatic Abdominal Aortic Aneurysm segmentation in MR images

Abdominal Aortic Aneurism is a disease related to a weakening in the aortic wall that can cause a break in the aorta and the death. The detection of an unusual dilatation of a section of the aorta is an indicative of this disease. However, it is difficult to diagnose because it is necessary image diagnosis using computed tomography or magnetic resonance. An automatic diagnosis system would allow to analyze abdominal magnetic resonance images and to warn doctors if any anomaly is detected. We focus our research in magnetic resonance images because of the absence of ionizing radiation. Although there are proposals to identify this disease in magnetic resonance images, they need an intervention from clinicians to be precise and some of them are computationally hard. In this paper we develop a novel approach to analyze magnetic resonance abdominal images and detect the lumen and the aortic wall. The method combines different algorithms in two stages to improve the detection and the segmentation so it can be applied to similar problems with other type of images or structures. In a first stage, we use a spatial fuzzy C-means algorithm with morphological image analysis to detect and segment the lumen; and subsequently, in a second stage, we apply a graph cut algorithm to segment the aortic wall. The obtained results in the analyzed images are pretty successful obtaining an average of 79% of overlapping between the automatic segmentation provided by our method and the aortic wall identified by a medical specialist. The main impact of the proposed method is that it works in a completely automatic way with a low computational cost, which is of great significance for any expert and intelligent system.

Long-Term Clinical and Imaging Follow-Up After Reinforced Pulmonary Autograft Ross Procedure.

The Ross operation remains a controversially discussed procedure when performed in the full root technique because concern exists regarding late dilatation of the pulmonary autograft and regurgitation of the neo-aortic valve. In 2008, we published our short-term experience when using external reinforcement of the autograft, which was inserted into a prosthetic Dacron graft. This detail was thought to prevent neoaortic root dilatation. Since 2006, 22 adult patients have undergone a Ross procedure using this technique. Indications were aortic regurgitation (n = 2), aortic stenosis (n = 15), and combined aortic stenosis and insufficiency (n = 5). A bicuspid aortic valve was present in 10 patients. Prior balloon valvuloplasty had been performed in seven patients. No early or late deaths occurred in this small series. One patient required aortic valve replacement early postoperatively, but freedom from late reoperation is 100% in the 21 remaining patients. Echocardiography confirmed the absence of more than trivial aortic insufficiency in 15 patients after a mean of 70 months (range, 14 to 108 months). No autograft dilatation was observed during follow-up and all patients are in New York Heart Association Class I. Autograft reinforcement is a simple and reproducible technical adjunct that may be especially useful in situations known for late autograft dilatation, namely, bicuspid aortic valve, predominant aortic insufficiency, and ascending aortic enlargement. The mid- to long-term results are encouraging because no late aortic root enlargement has been observed and the autograft valve is well functioning in all cases.

Les mécanismes sous-jacents aux effets pathologiques cardiaques de l’angiotensine II dans le remodelage électrique et contractile entre les sexes

L’insuffisance cardiaque (IC) est associée à un taux de mortalité et d’hospitalisations élevé causant un fardeau économique important. Les deux causes majeures de décès de l’IC sont les arythmies ventriculaires létales et les sidérations myocardiques. Il est maintenant reconnu que l’angiotensine II (ANGII) est l'un des principaux médiateurs de l’IC. Ses effets délétères découlent de l’activation du récepteur de type 1 de l’ANGII (AT1) et entraînent le développement d’hypertrophie. Toutefois, son rôle dans la genèse d’arythmies demeure incompris. De ce fait, l'étude des mécanismes électriques et contractiles sous-jacents aux effets pathologiques de l’ANGII s’avère essentielle afin de mieux comprendre et soigner cette pathologie. Il est souvent perçu que les femmes sont protégées envers les maladies cardiovasculaires. Cependant, le nombre total de femmes décédant d’IC est plus grand que le nombre d’hommes. Également, l’impact des facteurs de risque diffère entre chaque sexe. Ces différences existent, mais les mécanismes sous-jacents sont encore peu connus. De plus, les femmes reçoivent fréquemment un diagnostic ou un traitement inapproprié en raison d’un manque d’information sur les différences entre les sexes dans la manifestation d’une pathologie. Ce manque de données peut découler du fait que les sujets de sexe féminin sont souvent sous-représentés dans les essais cliniques ou la recherche fondamentale ce qui a grandement limité l’avancement de nos connaissances sur ~50 % de la population. Ainsi, il semble plus que nécessaire d’approfondir notre compréhension des différences entre les sexes, notamment dans la progression de l’IC. L’utilisation d’un modèle de souris transgénique surexprimant le récepteur AT1 (souris AT1R) a permis d’étudier les changements électriques, structurels et contractiles avant et après le développement d’hypertrophie. Premièrement, chez les souris AT1R mâles, un ralentissement de la conduction ventriculaire a été observé indépendamment de l’hypertrophie. Ce résultat était expliqué par une réduction de la densité du courant Na+, mais pas de l’expression du canal. Ensuite, le rôle des protéines kinases C (PKC) dans la régulation du canal Na+ par l’ANGII a été exploré. Les évidences ont suggéré que la PKCα était responsable de la modulation de la diminution du courant Na+ chez les souris AT1R mâles et dans les cardiomyocytes humains dérivés de cellules souches induites pluripotentes (hiPSC-CM) en réponse à un traitement chronique à l’ANGII. Ensuite, les différences entre les sexes ont été comparées chez la souris AT1R. Une plus grande mortalité a été constatée chez les femelles AT1R suggérant qu’elles sont plus sensibles à la surexpression de AT1R. Le remodelage électrique ventriculaire a donc été comparé entre les souris AT1R des deux sexes. Les courants ioniques étaient altérés de façon similaire entre les sexes excluant ainsi leur implication dans la mortalité plus élevée chez les femelles. Ensuite, l’homéostasie calcique et la fonction cardiaque ont été étudiées. Il a été démontré que les femelles développaient une hypertrophie et une dilatation ventriculaire plus sévère que les mâles. De plus, les femelles AT1R avaient de petits transitoires calciques, une extrusion du Ca2+ plus lente ainsi qu’une augmentation de la fréquence des étincelles Ca2+ pouvant participer à des troubles contractiles et à la venue de post-dépolarisations précoces. En conclusion, l’ANGII est impliquée dans le remodelage électrique, structurel et calcique associé à l'émergence de l’IC. De surcroît, ces altérations affectent plus sévèrement les femelles soulignant la présence de différences entre les sexes dans le développement de l’IC.