Reconstrucción de párpado inferior con injerto de cartílago auricular de espesor parcial y colgajo de la laguinge en doble banderín / Reconstruction of lower eyelid auricular cartilage graft split-thickness flap and double pennant Laguinge

El objetivo principal en la reconstrucción de párpados es promover una adecuada protección del globo ocular así como la restitución de sus planos anatómicos. En el caso a presentar, el paciente padecía un carcinoma basocelular en el borde libre del párpado inferior izquierdo, que comprometía su lámina anterior y posterior (figura 1). Para poder obtener una correcta estabilidad se decidió utilizar un injerto de cartílago auricular de espesor parcial con periocondrio para la reconstrucción del tarso (Matsuo, 1987; Friedhofer, 1999 y un colgajo en doble banderín de Laguinge para su cobertura. Se obtuvo la epitelización del injerto en tiempos estándares según la literatura y un buen resultado estético y funcional...

Role of voltage-gated L-type Ca2+ channel isoforms for brain function.

Voltage-gated LTCCs (L-type Ca2+ channels) are established drug targets for the treatment of cardiovascular diseases. LTCCs are also expressed outside the cardiovascular system. In the brain, LTCCs control synaptic plasticity in neurons, and DHP (dihydropyridine) LTCC blockers such as nifedipine modulate brain function (such as fear memory extinction and depression-like behaviour). Voltage-sensitive Ca2+ channels Cav1 .2 and Cav1.3 are the predominant brain LTCCs. As DHPs and other classes of organic LTCC blockers inhibit both isoforms, their pharmacological distinction is impossible and their individual contributions to defined brain functions remain largely unknown. Here, we summarize our recent experiments with two genetically modified mouse strains, which we generated to explore the individual biophysical features of Cav1.2 and Cav1.3 LTCCs and to determine their relative contributions to various physiological peripheral and neuronal functions. The results described here also allow predictions about the pharmacotherapeutic potential of isoform-selective LTCC modulators.

Signaling pathways of interleukin-1 actions in the brain: anatomical distribution of phospho-ERK1/2 in the brain of rat treated systemically with interleukin-1beta.

Interleukin-1beta is released at the periphery during infection and acts on the nervous system to induce fever, neuroendocrine activation, and behavioral changes. These effects are mediated by brain type I IL-1 receptors. In vitro studies have shown the ability of interleukin-1beta to activate mitogen-activated protein kinase signaling pathways including p38, c-Jun N-terminal kinase and extracellular signal-regulated protein kinase 1 and 2 (ERK1/2). In contrast to other mitogen-activated protein kinases, little is known about ERK1/2 activation in the rat brain in response to interleukin-1beta. The aim of the present study was therefore to investigate spatial and temporal activation of ERK1/2 in the rat brain after peripheral administration of interleukin-1beta using immunohistochemistry to detect the phosphorylated form of the kinase. In non-stimulated conditions, phosphorylated ERK1/2 immunoreactivity was observed in neurons throughout the brain. Administration of interleukin-1beta (60 microg/kg, i.p.) induced the phosphorylation of ERK1/2 in areas at the interface between brain and blood or cerebrospinal fluid: meninges, circumventricular organs, endothelial like cells of the blood vessels, and in brain nuclei involved in behavioral depression, fever and neuroendocrine activation: paraventricular nucleus of the hypothalamus, supraoptic nucleus, central amygdala and arcuate nucleus. Double labeling of phosphorylated ERK1/2 and cell markers revealed the expression of phosphorylated ERK1/2 in neurons, astrocytes and microglia. Since phosphorylated ERK1/2 was found in structures in which type I IL-1 receptor has already been identified as well as in structures lacking this receptor, activation of ERK1/2 is likely to occur in response to both direct and indirect action of interleukin-1beta on its target cells.

[Ventricular tachycardia in a patient with rate-responsive cardiac pacemaker]. / Tachycardie ventriculaire chez un porteur de stimulateur cardiaque à fréquence asservie.

The authors report a case of syncopal ventricular tachycardia in a patient with a respiratory-dependent rate responsive pacemaker, followed-up for valvular heart disease with severe left ventricular dysfunction and sustained atrial and ventricular arrhythmias. The introduction of low dose betablocker therapy with reinforcement of the treatment of cardiac failure controlled the ventricular arrhythmia, after suppression of the data responsive function had been shown to be ineffective. The authors discuss the role of the rate responsive function in the triggering of the ventricular tachycardias.

Clinical and ultrasound results after aortic valve replacement: intermediate-term follow-up with the St. Jude Medical prosthesis.

Mortality, morbidity, quality of life, and left ventricular (LV) function were evaluated in 49 patients after aortic valve replacement with the St. Jude prosthesis. Total follow-up was 2577 patient-months; survivors were followed-up for 4 to 7 years by clinical examination and echocardiography. The actuarial survival rate at 6 years was 79.6%, and there were no valve-related deaths. The linearized rates for thromboembolism and hemorrhage were 0.93% and 3.26% per patient-year, respectively. In 34% of the survivors the quality of life was poor. In the first three postoperative months, patients with aortic stenosis (n = 12) had a significant decrease in the muscle cross-sectional area (p less than 0.01) and patients with aortic regurgitation (n = 11) had decreases in both LV end-diastolic diameter (p less than 0.05) and cross-sectional area (p less than 0.001). All of these results were maintained at 5 years without modification of LV systolic function. Despite the good overall results, six patients deteriorated and had major LV dilatation. Multivariate logistic regression analysis identified two independent preoperative variables associated with a poor outcome defined as death of LV dysfunction (p less than 0.05): age and end-diastolic diameter. Thus meticulous follow-up showed a high incidence of hemorrhage and a poor quality of life in many of the survivors. It was concluded that in high-risk patients (age and end-diastolic diameter) surgery should probably be considered earlier.

[Doppler ultrasound evaluation of aortic insufficiency using half-pressure time. Absence of arterial rigidity influence]. / Evaluation doppler de l'insuffisance aortique par le temps de demi-pression. Absence d'influence de la rigidité artérielle.

In 20 patients with pure aortic regurgitation we studied the relationship between the severity of regurgitation, as assessed haemodynamically by the percentage of leakage (%L), and the half-pressure (T 1/2 P) and half-velocity (T 1/2 V) times, as obtained from doppler aortic blood velocity curves, taking into account the rigidity of the systemic vascular circuit characterized by the pressure wave propagation velocity (PWPV). The systemic arterial circuit was supple in 14 patients (PWPV less than 7.5 m/sec) and rigid in 6 patients (PWPV greater than 7.5 m/sec). The regression slopes between %L and T 1/2 P and between %L and T 1/2 V were calculated with their confidence limits in the 14 patients with supple arteries. The 6 patients with rigid arteries fitted into this nomogram, thus demonstrating that systemic arterial rigidity makes no difference in the relationship between %L and doppler indices. The half-velocity and half-pressure times measured by doppler ultrasound were acquired from a velocity signal directly determined by the aortic regurgitation, without any detectable effect of vascular circuit rigidity. Being equivalent by nature to the signal decrease time constant, they are independent of the absolute protodiastolic value of diastolic pressure gradient or blood flow velocity. For this reason these two doppler parameters are reliable to evaluate the severity of aortic regurgitation.