Browsing by Author "Del Rio, R."

Now showing 1 - 6 of 6
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    A potentiostatic and atomic force Microscopy study of the nucleation and growth mechanisms of certain metallic cyanometalates
    (AMER CHEMICAL SOC, 2007) Orellana, M.; Del Rio, R.; Schrebler, R.; Cordova, R.
    Nucleation and growth mechanisms (NGMs) of nickel(II) hexacyanoferrate, nickel(II) octacyanomolibdate, and copper(II) octacyanomolibdate were performed by means of the potential step technique by oxidizing the respective metal electrode in 0.02 M sulfuric acid containing the potassium salt of either hexacyanoferrate or octacyanomolibdate compounds. The obtained current-time transients (I/t) were analyzed using the theory of electrocrystallization of the metallic phase. As evidenced through these experiments, we can state that for the nickel cyanometalate compounds, electroformation takes place through a three-dimensional progressive NGM, and for the copper(II) octacyanomolibdate compound, electroformation occurs by means of a three-dimensional instantaneous NGM. The electrochemical results were verified through the use of atomic force microscopy (AFM). From these results, we can conclude that AFM is a good complementary technique to determine the nature of the NGMs through which electroformation of a solid phase occurs on an electrode surface.
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    Acute Chemogenetic Inhibition of Caudal NTS Astrocytes Reduced Systemic Blood Pressure in Rats Exposed to Chronic Intermittent Hypoxia-mimicking Sleep Apnea Syndrome
    (NLM (Medline), 2022) Iturriaga, R.; Toledo, C.; Ortolani, D.; Del Rio, R.
    © FASEB.Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) discharges, leading to heightened sympathetic outflow and systemic hypertension. Previously, we found that CBs play a pivotal role in the hyperactivation of central nervous system (CNS) autonomic nuclei following CIH, particularly at the level of the caudal portion of the nucleus of the tractus solitary (NTS). Indeed, increased CB afferent activity during CIH increases the expression of pro-inflammatory cytokines in the NTS, suggesting that CBs may drive neuroinflammation at key cardiorespiratory regulatory areas. Astrocytes has been implicated in inflammatory processes at the CNS. However, the contribution of NTS astrocytes on the cardiorespiratory abnormalities following CIH has not been studied. Accordingly, we assessed the role of astrocytes residing within the NTS on the maintenance of hypertension following CIH. Male Sprague-Dawley rats (200 g) were exposed to CIH (5-6% inspired O2 for 20s, followed by room air for 280s, 12 times/h, 8 h/day, for 28 days). Arterial blood pressure (BP) was measured by indwelling telemetry. At 7 days of CIH exposure, rats were anesthetized and an adeno-associated virus (AAV; 450 nL, 1*10-12 vg) containing an inhibitory (Gi) Designer Receptor Exclusively Activated by Designer Drugs (DREADD) expressed under the control of the GFAP promoter was bilaterally injected into the caudal portion of the NTS using stereotaxic coordinates (-14.3 mm to bregma). At day 28 of CIH, hemodynamic and respiratory parameters were recorded before and after inhibition of NTS astrocytes with clozapine N-oxide (CNO, 1mg/kg, ip.). At the end of the experiments rats were transcardially perfused with 4% buffered paraformaldehyde, brains extracted and sectioned to assess astrocyte activation within the NTS. Twenty-eight days of CIH resulted in a significant 2-fold increase in NTS astrocyte activation as evidenced by enhanced reactivity of GFAP. Additionally, resting BP was markedly elevated compared to Sham conditions (MABP, 98±2 vs. 84±2 mmHg, CIH vs. Sham; p<0.05). Acute chemogenetic inhibition of NTS astrocytes following 28 days of CIH results in a significant reduction in BP (⁓10 mmHg; p<0.05). In addition, the exacerbated hemodynamic response triggered by acute hypoxic stimulation (Fi O2 10%) in rats exposed to CIH for 28 days was also reduced by NTS astrocyte inhibition ΔMABP, 30±2 vs. 15±2 mmHg, pre vs. post CNO; p<0.05). No cardiovascular effects of CNO alone were found in control rats that did not underwent AAV-DREADD-Gi injection into the NTS. Taken together, our results support a role for NTS astrocyte activation on the maintenance of hypertension following chronic CIH and suggest that activation of NTS astrocytes may participate in the CB-mediated cardiovascular reflex response during hypoxic stimulation.
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    Heart rate variability alterations in infants with spontaneous hypertonia
    (2019) Arce-Alvarez, A.; Melipillan, C.; Andrade Andrade, David Cristóbal; Toledo, C.; Marcus, N.J.; Del Rio, R.
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    Kinematic and Neuromuscular Measures of Intensity During Plyometric Jumps
    (2017) Andrade Andrade, David Cristóbal; Manzo, O.; Beltran, A.; Álvarez, C.; Del Rio, R.; Toledo, C.; Moran, J.; Ramirez Campillo, R.
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    Neurocognitive Disorders in Heart Failure: Novel Pathophysiological Mechanisms Underpinning Memory Loss and Learning Impairment
    (SPRINGER, 2019) Toledo, C.; Andrade, D. C.; Diaz, H. S.; Inestrosa, N. C.; Del Rio, R.
    Heart failure (HF) is a major public health issue affecting more than 26 million people worldwide. HF is the most common cardiovascular disease in elder population; and it is associated with neurocognitive function decline, which represent underlying brain pathology diminishing learning and memory faculties. Both HF and neurocognitive impairment are associated with recurrent hospitalization episodes and increased mortality rate in older people, but particularly when they occur simultaneously. Overall, the published studies seem to confirm that HF patients display functional impairments relating to attention, memory, concentration, learning, and executive functioning compared with age-matched controls. However, little is known about the molecular mechanisms underpinning neurocognitive decline in HF. The present review round step recent evidence related to the possible molecular mechanism involved in the establishment of neurocognitive disorders during HF. We will make a special focus on cerebral ischemia, neuroinflammation and oxidative stress, Wnt signaling, and mitochondrial DNA alterations as possible mechanisms associated with cognitive decline in HF. Also, we provide an integrative mechanism linking pathophysiological hallmarks of altered cardiorespiratory control and the development of cognitive dysfunction in HF patients.
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    Singular rank one perturbations
    (2022) Astaburuaga, M. A.; Cortes, V. H.; Fernandez, C.; Del Rio, R.
    In this paper, A = B + V represents a self-adjoint operator acting on a Hilbert space H. We set a general theoretical framework and obtain several results for singular perturbations of A of the type A(beta) = A + beta tau*tau for tau being a functional defined in a subspace of H. In particular, we apply these results to H-beta = -Delta + V + beta|delta >