707 research outputs found

    Magnetic Resonance Imaging in patients with ICDs and Pacemakers

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    Magnetic resonance (MR) imaging has unparalleled soft-tissue imaging capabilities. The presence of devices such as pacemakers and implantable cardioverter/defibrillators (ICDs), however, is historically considered a contraindication to MR imaging. These devices are now smaller, with less magnetic material and improved electromagnetic interference protection. This review summarizes the potential hazards of the device-MR environment interaction, and presents updated information regarding in-vivo and in-vitro experiments. Recent reports on patients with implantable pacemakers and ICDs who underwent MR scan shows that under certain conditions patients with these implanted systems may benefit from this imaging modality. The data presented suggests that certain modern pacemaker and ICD systems may indeed be MR safe. This may have major clinical implications on current imaging practice

    Coronary Aneurysm Occurring Late after Drug-Eluting Stent Implantation

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    Drug-eluting stents may affect the normal healing process of the vessel wall and the remodeling process and may lead to late stent malapposition (LSM). The known incidence of this phenomen originates from short-term angiographic follow-up studies. We describe a case report of very late stent malapposition and marked positive vessel remodeling 3 years after sirolimus-eluting coronary stent implantation. Angiography performed one year after stent implantation was normal. Thus, the abnormalities developed sometime between years 1 and 3. The cause is unknown, but it is reasonable to suggest a local effect of the medication/polymer of the stent. LSM rate and aneurysmal formation is higher in DES than in BMS and may be associated with increased risk for late stent thrombosis. Currently, the risk of very late stent thrombosis after DES implantation is of major concern. As observed in this case report, LSM might occur and develop very late. This has significant consequences especially to the many asymptomatic patients with DES implanted many years ago and the recommendation of dual antiplatelet therapy. More studies with late and very late follow up are needed to better define this finding, its mechanism, how to avoid it, and how to treat it properly

    Magnetic Resonance Imaging in patients with ICDs and Pacemakers

    Get PDF
    Magnetic resonance (MR) imaging has unparalleled soft-tissue imaging capabilities. The presence of devices such as pacemakers and implantable cardioverter/defibrillators (ICDs), however, is historically considered a contraindication to MR imaging. These devices are now smaller, with less magnetic material and improved electromagnetic interference protection. This review summarizes the potential hazards of the device-MR environment interaction, and presents updated information regarding in-vivo and in-vitro experiments. Recent reports on patients with implantable pacemakers and ICDs who underwent MR scan shows that under certain conditions patients with these implanted systems may benefit from this imaging modality. The data presented suggests that certain modern pacemaker and ICD systems may indeed be MR safe. This may have major clinical implications on current imaging practice

    Crosstalk between ROS-dependent apoptotic and autophagic signaling pathways in Zn(II) phthalocyanine photodynamic therapy of melanoma

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    Melanoma is the most aggressive type of skin cancer, highly resistant to conventional therapies. Photodynamic therapy (PDT) is a minimally invasive treatment modality that combines the use of a photosensitizer, visible light and molecular oxygen, leading to ROS generation in the specific site of irradiation. The cationic zinc(II) phthalocyanine Pc13 has shown to be a potent photosensitizer in different melanoma cell lines. In this study, we explored the intracellular signaling pathways triggered by Pc13 PDT and the role of these cascades in the phototoxic action of Pc13 in human melanoma A375 cells. ROS-dependent activation of MAPKs p38, ERK, JNK and PI3K-I/AKT was observed after treatment. Inhibition of p38 reduced Pc13 phototoxicity, whereas blockage of ERK did not affect this response. Conversely, JNK inhibition potentiated the effect of Pc13 PDT. Results obtained indicate that p38 is involved in the cleavage of PARP-1, an important mediator of apoptosis. On the other hand, Pc13 irradiation induced the activation of an autophagic program, as evidenced by enhanced levels of Beclin-1, LC3-II and GFP-LC3 punctate staining. We also demonstrated that this autophagic response is promoted by JNK and negatively regulated by PI3K-I/AKT pathway. The blockage of autophagy increased Pc13 phototoxicity and enhanced PARP-1 cleavage, revealing a protective role of this mechanism, which tends to prevent apoptotic cell death.Furthermore, reduced susceptibility to treatment and increased activation of autophagy were detected in A375 cells submitted to repeated cycles of Pc13 PDT, indicating that autophagy could represent a mechanism of resistance to PDT. The efficacy of Pc13 PDT and an improved phototoxic action in combination with chloroquine were also demonstrated in tumor spheroids. In conclusion, we showed the interplay between apoptotic and autophagic signaling pathways triggered by Pc13 PDT-induced oxidative stress. Thus, autophagy modulation represents a promising therapeutic strategy to potentiate the efficacy of PDT in melanoma.Fil: Valli, Federico. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y BioquĂ­mica. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas; ArgentinaFil: Garcia Vior, MarĂ­a Cecilia. Universidad de Buenos Aires. Facultad de Farmacia y BioquĂ­mica. Departamento de QuĂ­mica OrgĂĄnica; Argentina. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas; ArgentinaFil: Roguin, Leonor Patricia. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y BioquĂ­mica. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas; ArgentinaFil: Marino, Veronica Julieta. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y BioquĂ­mica. Instituto de QuĂ­mica y FĂ­sico-QuĂ­mica BiolĂłgicas; Argentin

    Quand le divin Achille se met Ă  penser : colĂšre, dĂ©sespoir et pitiĂ© dans l’Iliade

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    La colĂšre d’Achille qui, selon le proĂšme de l’Iliade, cause d’innombrables maux pour les AchĂ©ens, rĂ©sulte de l’affront qu’Agamemnon fait Ă  Achille en lui prenant BrisĂ©is. Mais aprĂšs la mort de Patrocle, Achille Ă©prouve un courroux plus grand encore, cette fois envers Hector et les Troyens. Dans cet article, on s’intĂ©resse moins Ă  la colĂšre d’Achille qu’au processus par lequel celui-ci renonce Ă  sa colĂšre. Ce processus repose sur un travail de rĂ©flexion, auquel se livre Achille Ă  diffĂ©rents endroits du poĂšme, et dont une partie dĂ©terminante se produit au moment oĂč il accomplit les funĂ©railles de Patrocle. ProfondĂ©ment affligĂ©, conscient de l’imminence de sa mort, il se montre sensible aux souffrances de Priam, venu lui racheter le corps d’Hector.Achilles’ anger, which according to the proem of the Iliad causes countless sufferings for the Achaeans, begins when Agamemnon slights Achilles in seizing upon Briseis. But after Patroclus’ death, Achilles is still more angry, this time against Hector and the Trojans. In this paper, emphasis is laid less on Achilles’ anger than on the process through which Achilles gives up his anger. This is a process of thought, to which Achilles devotes himself at different points of the narrative. An important part of it occurs during Patroclus’ funeral. Deeply grieved, aware of his impending death, Achilles is then capable of understanding the sufferings of Priam, who comes to him to buy back Hector’s corpse

    High prevalence of muscular ventricular septal defect in neonates

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    Objectives.This study sought to use echocardiography to evaluate the prevalence of muscular ventricular septal defect in neonates.Background.Ventricular septal defect is usually asymptomatic and closes spontaneously. An increase in its prevalence has been noted recently. One reason is the improved detection of small defects, especially with the increased use of echocardiography. Therefore, one would expect a higher prevalence in neonates on the basis of echocardiographic screening.Methods.Color Doppler echocardiography was performed in 1,053 consecutive neonates 6 to 170 h old at Western Galilee Hospital, Israel. Data on the neonates, parents and family were obtained to analyze the influencing factors. The identified patients were followed up for 1 to 10 months or until ventricular septal defect closure.Results.Muscular ventricular septal defect was found in 56 (25 male, 31 female) of the 1,053 neonates, a prevalence of 53.2/1,000 live births. All neonates were asymptomatic. Six had a systolic murmur. Electrocardiographic findings were normal in 44 (97.8%) of 45 neonates followed up, and left ventricular hypertrophy occurred in 1 (2.2%). By echocardiography, 50 ventricular septal defects (89.3%) were single and 6 (10.7%) were multiple. The defects (range 1 to 5 mm in diameter, mean [±sd]2.3 ± 0.8) occurred anywhere along the muscular septum; 43 (76.8%) were detectable only on color Doppler imaging. The left atrium and left ventricle were mildly dilated. Of 45 neonates who were followed up for 6 to 10 months or until closure of the defects, 40 (88.9%) had defects that closed spontaneously. The risk of ventricular septal defect was not significantly associated with gestational age, birth weight, birth order, maternal age, diabetes, smoking, exposure to drugs or infection, paternal age, familial congenital heart disease, religion or consanguinity.Conclusions.There is a prevalence of muscular ventricular septal defect in neonates of 53.2/1,000 live births. The patients were asymptomatic, and 88.9% had defects that closed spontaneously within 1 to 10 months. These defects may be caused by environmental factors. In many cases, muscular ventricular septal defect may also result from delayed physiologic development
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