Biomedical subjects

Armando Mansilla-Olivares

Publications and source records attributed to Armando Mansilla-Olivares.

3 recordsLinked to original sources

PubMedDate not supplied

[Ultrastructural findings during human myocardial preservation with HTK solution].

Although the majority of recent scientific advances developed in the field of myocardial preservation have improved surgery procedures, it seems that during cardiothoracic surgery ischemia-reperfusion continues triggering clinical postoperative problems. This report focused on the changes human capillary endothelial cells and nerve endings suffer after cardiopulmonary bypass. The study involved four patients who received Bretschneider solution for cardioplegia during mitral stenosis surgery. Biopsies of right atrium were taken prior to and after CPB to be analyzed under electron microscopy. Samples taken after CPB showed detachment of myocardial capillary basal membrane, endothelial edema, and widespread nerve-ending destruction. Nevertheless, the shelter provided by the most advanced cardioplegic solutions, myocardial endothelial edema, and nerve-ending destruction cannot be completely prevented. Thus, it is possible to suggest that low interstitial concentration of Na(+), which activates Na(+)/Ca(++) exchanger, and inflow of Ca(++), present during ischemia-reperfusion, may lead to endothelial and neuronal cell damage, triggering cardiac contraction dysfunction. This mechanism would explain at least in part some of the problems patients face during the postoperative state.

Adult↗

PubMedDate not supplied

[Calcium, the atom triggering life and cellular function].

Although during the last three decades phosphorylation and dephosphorylation systems have been pointed out as the mechanisms used by living cells to control biological processes, it seems that calcium dynamics is the phenomenon that precedes and controls protein activation by the introduction of phosphate groups into distinct protein structures. The process begins with activation of calcium channels that allows the influx of the ion, which once inside the cell leads to calcium-calmodulin complex, a molecule capable of triggering activation of distinct proteinkinases. Thus, the cell in addition to suffering a change in polarity enhances neuroconduction and release of different substances such as hormones and para-hormones, facilitates intra- and intercellular communication, and exerts determinant influence on phenotypic expression by means of promotion of immediate and mediate response genes. Ionic conformational calcium runs short- and long-term facilitation mechanisms, exerting its influence on control of memory through homosynaptic depression and hetersynaptic facilitation processes; triggers autophosphorylation of several enzymes leading and enhancing cellular activity and participates in signal transduction and decodification. Calcium influx rate activates certain groups of phosphatases capable of inhibiting autophosphorylation processes, only as a negative feedback mechanism. In addition, ionic calcium also participates in the "cross-activate" mechanism of proteinkinases A and G, influencing to production of systemic and central nervous system nitric oxide. On these bases, it is possible to guess that future pharmacologic interventions on calcium fluxes could be of invaluable importance in prevention and control of a number of distinct physiopathologic events.

Animals↗

PubMedDate not supplied

[Signal transduction, pillar of the neurobiological integration of memory. An alternative view to the cholinergic hypothesis].

Neurophysiological, biochemical and molecular processes described in the integration of memory are closely related with neurotransmitters such as glutamate and serotonin (SHT) and with the function of calcium and potassium ion channels more than with cholinergic activity. Infact, glutamate and 5-HT receptors are closely related with Long-Term potentiation (L TP) processes, the mechanism by which memory is preserved throughout time. That is, the activation of the 5-HTI receptor triggers a transduction signal that after influencing nuclear cell activity, provokes several presynaptic changes, which leads to the displacement of magnesium from the postsynaptic area depolarizing the neuron and leading to the activation of N-methyl-D-aspartate receptors (NMDA). As a whole, this process contributes to the support and perpetuation of LTP, which consists of the following processes: LTPI that depends on protein kinase activity; LTP2 linked to translation of genes; and LTP3 closely related to genes transcription. On the opposite side but in perfect balance, we find the mechanism of Long-Term depression (LTD), which is triggered instead when the Ca+ +flow decreases in the presynaptic neuron activating the inhibitor-1 enzyme that promotes the dephosphorylation of a calmodulin-dependent protein kinasell and as a result, the inhibition of autophosphorylation and consequently of LTP too. Despite the widespread dissemination of the cholinergic hypothesis in Alzheimer's disease, memory build up rather than involving acetylcholine essentially depends on the participation of other neurotransmitters such as 5-HT and glutamate, which have not been adequately considered in the treatment of this disease. However, beyond neurotransmission, it is the cellular mechanism of autophosphorylation of several protein kinases, the process susceptible of being activated or controlled by the action of distinct substances. In such a case, it would be possible to exert some influence on gene expression improving perhaps, some of the physiopathological deficits that characterize memory disruption.

Calmodulin↗