Imagerie dans le cathétérisme des cardiopathies congénitales : place de l’échocardiographie 3D transthoracique

RésuméL’échocardiographie 3D transthoracique a longtemps été freinée dans son développement en raison de conditions techniques d’acquisition compliquées et de qualité d’images médiocres. L’avènement des sondes matricielles permet au 3D en devenant temps réel d’entrer dans la pratique clinique courante. Si la voie œsophagienne a permis au 3D de trouver ses lettres de noblesses par ses descriptions anatomiques uniques des valves et des septa, l’échocardiographie transthoracique peut désormais se décliner en modes 2D, Doppler et 3D. Ses applications dans la cardiologie congénitale et pédiatrique sont multiples : description anatomique précise des défauts septaux auriculaires et ventriculaires, classification des bicuspidies aortiques et analyse du mécanisme de sténose. Ainsi, l’échocardiographie 3D permet-elle de sélectionner de façon non invasive les patients, de guider et de juger du résultat d’un cathétérisme interventionnel. L’imagerie 3D est un excellent moyen de communication entre l’imageur et le cardiologue interventionnel mais aussi de délivrer des informations claires au patient et à la famille avant et après un cathétérisme.SummaryThree-dimensional echocardiography has improved dramatically due to technical advances in probe design and computer processing. The introduction of real time 3D echocardiography has led to its use in everyday clinical practice. Congenital heart disease demands a detailed understanding of the spatial relationships of cardiac structures to plan treatment. The introduction of new transthoracic 3D probes has extended the applications to real-time guidance of catheter procedures. Prominent among the cardiac lesions which have been studied are: atrial septal defects, ventricular septal defects and stenotic bicuspid aortic valves. Its values should be decisive in many congenital cardiac lesions requiring interventional catheterisation. 3D echocardiography is an easy way to communicate to the patient and its family about the pathology

Presynaptic Nicotinic α7 and Non-α7 Receptors Stimulate Endogenous GABA Release from Rat Hippocampal Synaptosomes through Two Mechanisms of Action

BACKGROUND: Although converging evidence has suggested that nicotinic acetylcholine receptors (nAChR) play a role in the modulation of GABA release in rat hippocampus, the specific involvement of different nAChR subtypes at presynaptic level is still a matter of debate. In the present work we investigated, using selective α7 and α4β2 nAChR agonists, the presence of different nAChR subtypes on hippocampal GABA nerve endings to assess to what extent and through which mechanisms they stimulate endogenous GABA release. METHODOLOGY/FINDINGS: All agonists elicited GABA overflow. Choline (Ch)-evoked GABA overflow was dependent to external Ca(2+), but unaltered in the presence of Cd(2+), tetrodotoxin (TTX), dihydro-β-erythroidine (DHβE) and 1-(4,4-Diphenyl-3-butenyl)-3-piperidinecarboxylic acid hydrochloride SKF 89976A. The effect of Ch was blocked by methyllycaconitine (MLA), α-bungarotoxin (α-BTX), dantrolene, thapsigargin and xestospongin C, suggesting that GABA release might be triggered by Ca(2+) entry into synaptosomes through the α7 nAChR channel with the involvement of calcium from intracellular stores. Additionally, 5-Iodo-A-85380 dihydrochloride (5IA85380) elicited GABA overflow, which was Ca(2+) dependent, blocked by Cd(2+), and significantly inhibited by TTX and DHβE, but unaffected by MLA, SKF 89976A, thapsigargin and xestospongin C and dantrolene. These findings confirm the involvement of α4β2 nAChR in 5IA85380-induced GABA release that seems to occur following membrane depolarization and opening calcium channels. CONCLUSIONS/SIGNIFICANCE: Rat hippocampal synaptosomes possess both α7 and α4β2 nAChR subtypes, which can modulate GABA release via two distinct mechanisms of action. The finding that GABA release evoked by the mixture of sub-maximal concentration of 5IA85380 plus sub-threshold concentrations of Ch was significantly larger than that elicited by the sum of the effects of the two agonists is compatible with the possibility that they coexist on the same nerve terminals. These findings would provide the basis for possible selective pharmacological strategies to treat neuronal disorders that involve the dysfunction of hippocampal cholinergic system

Genetic Basis of Myocarditis: Myth or Reality?

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Decreased dopaminergic inhibition of pyramidal neurons in anterior cingulate cortex maintains chronic neuropathic pain

Pyramidal neurons in the anterior cingulate cortex (ACC), a prefrontal region involved in processing the affective components of pain, display hyperexcitability in chronic neuropathic pain conditions, and their silencing abolishes hyperalgesia. We show that dopamine, through D1 receptor (D1R) signaling, inhibits pyramidal neurons of mouse ACC by modulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. Activation of Gs-coupled D1R by dopamine induces the opening of HCN channels at physiological membrane potentials, driving a significant decrease in input resistance and excitability. Systemic L-DOPA in chronic neuropathic mice rescues HCN channel activity, normalizes pyramidal excitability in ACC, and blocks mechanical and thermal allodynia. Moreover, microinjection of a selective D1R agonist in the ACC relieves the aversiveness of ongoing neuropathic pain, while an ACC D1R antagonist blocks gabapentin- and lidocaine-evoked antinociception. We conclude that dopaminergic inhibition via D1R in ACC plays an analgesic role in physiological conditions and is decreased in chronic pain. © 2021 The AuthorsOpen access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Effect of Stretching on the Structure of Cylinder- and Sphere-Forming Styrene-Isoprene-Styrene Block Copolymers

Two styrene-isoprene-styrene block copolymers Vector 4111 and 4113, exhibiting cylindrical (18 wt % PS) and spherical (16 wt % PS) morphology, respectively, have been examined under uniaxial elongation up to 200% strain. On the basis of stress-strain data, mechanical properties are compared for isotropic and oriented polystyrene domains. The structure at various stages of deformation has been determined from SAXS patterns in three planes and two principal deformation directions with respect to orientation. Samples showed a very high degree of hexagonal packing, resulting in an X-ray pattern taken parallel to the cylinder alignment approaching single crystal ordering. Cylinders were aligned with the closest packed planes parallel to film surface. Particular attention has been paid to a lattice deformation process occurring during the first stretching and relaxation cycle. For a copolymer with oriented cylindrical morphology the deformation was affine up to 120% strain. The microdomain spacing was calculated parallel and perpendicular to the stretching direction. The cylindrical microstructure orientation, quantified by Hermans' orientation factor reduced during elongation of oriented polymer, while the elongation of isotropic sample caused an increase of orientation. Deformation of all studied morphologies was reversible

Functional characterization of the P2X(4) receptor orthologues

1. The aim of this study was to functionally characterize the recombinant mouse P2X(4) receptor and to compare its pharmacological properties with those of the human and rat orthologues. 2. Whole cell recordings were made from rafts of HEK-293 cells stably expressing recombinant mouse, rat or human P2X(4) receptors, using Cs-aspartate containing electrodes (3–8 MΩ) in a HEPES-buffered extracellular medium. 3. The agonist potency of ATP at the three species orthologues was similar, with mean EC(50) values of 2.3 μM, 1.4 μM and 5.5 μM, respectively. 4. Adenosine-5′-tetraphosphate (AP4) acted as a partial agonist with respect to ATP at the mouse and human P2X(4) receptors (EC(50)=2.6 and 3.0 μM), but was significantly less potent at the rat orthologue (EC(50)=20.0 μM). α,β-methylene adenosine-5′-triphosphate (α,β-meATP) also acted as a partial agonist, producing 29% of the maximum response at the mouse P2X(4) and 24% at the human P2X(4) receptor. 5. In contrast to the other species orthologues, α,β-meATP failed to elicit a significant agonist response at rat P2X(4) receptors, and was found to act as an antagonist, with an IC(50) of 4.6 μM, against 10 μM ATP. 6. Mouse P2X(4) receptors were found to be sensitive to the antagonist, pyridoxalphosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) (IC(50)=10.5 μM), as were human P2X(4) receptors (IC(50)=9.6 μM). The rat receptor however, showed a low sensitivity to PPADS (IC(50)>100 μM). 7. All three orthologues were relatively suramin-insensitive (IC(50)>100 μM) and insensitive to 1-[N,O-Bis(5-isoquinoline sulphonyl)benzyl]-2-(4-phenylpiperazine)ethyl]-5-isoquinoline sulphonamide (KN-62; IC(50)>3 μM). 8. Our results suggest that the pharmacological properties of the mouse receptor are most similar to the human P2X(4) receptor, and differ markedly from the rat receptor