The Diagnostic Accuracy of Transvaginal Ultrasound for Detection of Ureteral Involvement in Deep Infiltrating Endometriosis: A Systematic Review and Meta-Analysis.

OBJECTIVE: The aim of this study is to determine the accuracy of transvaginal ultrasound (TVU) for the diagnosis of ureteral involvement in women with deep infiltrating endometriosis (DIE). METHODS: The meta-analysis included primary studies comparing the use of TVU for diagnosing endometriotic involvement of the ureter, using laparoscopic surgery and histological diagnosis as the reference standard. Search was performed in several databases (Scopus, Web of Science, and PubMed/MEDLINE). The studies' quality and bias risk were assessed using the Quality Assessment of Diagnostic Accuracy Study-2 (QUADAS-2). Diagnostic performance was estimated by assessing pooled sensitivity and specificity. RESULTS: A total of 496 citations were found. Six articles were ultimately selected for this systematic review and meta-analysis after the inclusion and exclusion criteria were applied. Pooled sensitivity and specificity were 0.81 (95% CI: 0.42-0.96), 1.00 (95% CI: 0.93-1.00). The heterogeneity observed was high for both sensitivity and specificity. Overall risk of bias was low. CONCLUSION: TVU is a valuable tool for the pre-operative identification of ureteral involvement by DIE.

Identification of Non-excitatory Amino Acids and Transporters Mediating the Irreversible Synaptic Silencing After Hypoxia.

The contribution of excitatory amino acids (AA) to ischemic brain injury has been widely described. In addition, we reported that a mixture of non-excitatory AA at plasmatic concentrations turns irreversible the depression of synaptic transmission caused by hypoxia. Here, we describe that the presence of seven non-excitatory AA (L-alanine, L-glutamine, glycine, L-histidine, L-serine, taurine, and L-threonine) during hypoxia provokes an irreversible neuronal membrane depolarization, after an initial phase of hyperpolarization. The collapse of the membrane potential correlates with a great increase in fiber volley amplitude. Nevertheless, we show that the presence of all seven AA is not necessary to cause the irreversible loss of fEPSP after hypoxia and that the minimal combination of AA able to provoke a solid, replicable effect is the mixture of L-alanine, glycine, L-glutamine, and L-serine. Additionally, L-glutamine seems necessary but insufficient to induce these harmful effects. We also prove that the deleterious effects of the AA mixtures on field potentials during hypoxia depend on both the identity and concentration of the individual AA in the mixture. Furthermore, we find that the accumulation of AA in the whole slice does not determine the outcome caused by the AA mixtures on the synaptic transmission during hypoxia. Finally, results obtained using pharmacological inhibitors and specific substrates of AA transporters suggest that system N and the alanine-serine-cysteine transporter 2 (ASCT2) participate in the non-excitatory AA-mediated deleterious effects during hypoxia. Thus, these AA transporters might represent therapeutical targets for the treatment of brain ischemia.

Hypoxia-induced depression of synaptic transmission becomes irreversible by intracellular accumulation of non-excitatory amino acids.

The intracellular accumulation of some amino acids (AAs), mainly glutamine, can contribute to brain edema observed during liver failure. We recently demonstrated that individual applications of high concentrations (10 mM) of some non-excitatory AAs increase the electrical resistance of hippocampal slices, indicating cell swelling. Therefore, we pondered whether an AA mixture's application might cause cell swelling at a physiological concentration range. In rat hippocampal slices, we carried out extra- and intracellular electrophysiological recordings and AAs analysis to address this question. We applied a mixture of 19 AAs at their plasmatic concentrations (Plasma solution: Ala, Gly, Gln, His, Ser, Tau, Thr, Arg, Leu, Met, Pro, Val, Asn, Cys, Phe, Ile, Lys, Tyr, and Trp). This solution was afterward divided into two according to the individual AAs at 10 mM concentration inducing synaptic potentiation (Plasma1, containing the first seven AAs of Plasma) or not (Plasma2, with the remaining AAs). Plasma application increased evoked field potentials requiring extracellular chloride. This effect was mimicked by the Plasma1 but not the Plasma2 solution. Plasma1-induced potentiation was independent of changes in release probability, basic electrophysiological membrane properties, and NMDAR activation. AAs in Plasma1 act cooperatively to accumulate intracellularly and to induce synaptic potentiation. In the presence of Plasma1, the reversible synaptic depression caused by a 40-min hypoxia period turned into an irreversible disappearance of synaptic potentials through an NMDAR-dependent mechanism. The presence of a system A transport inhibitor did not block Plasma1-mediated effects. These results indicate that cell swelling, induced by the accumulation of non-excitotoxic AAs through unidentified transporters, might foster deleterious effects produced by hypoxia-ischemia episodes.

Intracellular accumulation of amino acids increases synaptic potentials in rat hippocampal slices.

The application of high concentrations of taurine induces long-lasting potentiation of synaptic responses and axon excitability. This phenomenon seems to require the contribution of a transport system with a low affinity for taurine. The prototypic taurine transporter TauT (SLC6A6) was discarded by experimental evidence obtained in TauT-KO mice. The purpose of the present study was to determine whether the proton-coupled amino acid transporter 1 (PAT1; SLC36A1) which is a transport system with low affinity and high capacity for a great variety of amino acids including taurine, contributes to the taurine-induced synaptic potentiation. In rat hippocampal slices, the application of several amino acids (L- and D-alanine, L-glutamine, ß-guanidinopropionic acid, glycine, L-histidine, L- and D-serine, sarcosine, L- and D-threonine) imitated the synaptic potentiation induced by taurine. The magnitude of the potentiation caused by some of these amino acids was even greater than that induced by taurine. By contrast, the application of other amino acids (L-arginine, betaine, L-leucine, L-methionine, L- and D-proline, and L-valine) did not induce potentiation. The behaviour of these different amino acids on synaptic potentiation is not compatible with a role of PAT1 in synaptic potentiation. There was a positive correlation between the accumulation of the different amino acids in the slice and the magnitude of synaptic potentiation induced by them. Some of the amino acids inducing synaptic potentiation, like taurine and L-threonine, also increased electrical resistance of the slice, whereas L-leucine did not modify this parameter. Modifications induced by either taurine or L-threonine in synaptic potentiation, slice resistance and amino acid accumulation were dependent on extracellular chloride concentration. These findings support the idea that the accumulation of amino acids throughout the action of transporters causes cell swelling enhancing the electrical resistance of the slice, which by itself could be sufficient to increase field synaptic potentials.

Characterisation of the mechanisms underlying the special sensitivity of the CA2 hippocampal area to adenosine receptor antagonists.

Recent studies have underscored the importance of the CA2 area in social memory formation. This area, a narrow transition zone between hippocampal CA3 and CA1 areas, is endowed with special connectivity and a distinctive molecular composition. In particular, adenosine A1 receptors (A1R) are enriched in CA2, and based on the prominent synaptic potentiation induced by A1R antagonists (e.g., caffeine) in this area, it has been proposed that CA2 is under the strong tonic control of A1R activation. It is unclear whether this special sensitivity of CA2 to A1R antagonists is due to an elevated extracellular concentration of adenosine or to a different A1R function. Here, using the recording of field potentials evoked simultaneously in CA2 and CA1 by Schaffer collateral stimulation, we confirm that the application of A1R antagonists, caffeine and DPCPX has a stronger effect on synaptic responses in CA2 than in those evoked in CA1. This difference was, at least partially, explained by the action of A1R antagonists on presynaptic A1Rs. We found that caffeine-induced potentiation in CA2 was restricted to Schaffer collateral synapses, but not to those formed by temporoammonic inputs. We also observed that the apparent affinity of an A1R agonist is similar for A1R in both CA2 and CA1 areas, which indicates that the tonic activation of A1R in both areas is comparable. Furthermore, we show that the direct activation of adenylyl cyclase with forskolin in the presence of rolipram, a phosphodiesterase inhibitor, greatly enhances the synaptic potentials in CA2 compared to CA1. The forskolin-induced potentiation was exacerbated in the presence of caffeine or DPCPX, accentuating the differences between the two areas. These results indicate that the tonic activation of A1Rs in area CA2 is not different to that of other hippocampal areas, but it is more efficiently coupled to the downstream effectors.

Role of anxiety and brooding in specificity of autobiographical recall.

Overgeneral schemas and lack of autobiographical memory (AM) specificity about our past experiences can predict mood disturbance. Rumination, functional avoidance and executive processes are the main explanatory variables of such overgenerality. However, in non-clinical samples, rumination predicts overgenerality most consistently after the induction of dysphoric mood. Anxiety also activates rumination. Furthermore, anxiety predicts memory performance and has effects on mood which are independent of the effects of rumination. So, what might be the role of anxiety in autobiographical memory performance? A sample of 210 voluntary participants reported measures of autobiographical memory, anxiety, rumination (brooding and reflection), functional avoidance and executive functions (semantic and phonetic verbal fluency task). Autobiographical performance (specificity) was negatively associated with brooding and age and positively with phonetic verbal fluency but not with functional avoidance and anxiety. However, anxiety and brooding were positively correlated even after controlling for depression scores. Moreover, using structural equation modeling, anxiety showed a significant indirect effect on autobiographical specificity through brooding rumination. These results suggest a possible association of anxiety with autobiographical recall through brooding rumination.

The taurine transporter substrate guanidinoethyl sulfonate mimics the action of taurine on long-term synaptic potentiation.

Taurine is especially abundant in rodent brain where it appears to be involved in osmoregulation and synaptic plasticity mechanisms. The demonstration of a physiological role for taurine has been hampered by the difficulty in modifying taurine levels in most tissues, including the brain. We used an experimental strategy to reduce taurine levels, involving treatment with guanidinoethyl sulfonate (GES), a structural analogue of taurine that, among other properties, acts as a competitive inhibitor of taurine transport. GES delivered in the drinking water of rats for 1 month effectively reduced taurine levels in brain structures (hippocampus, cerebellum and cortex) and outside the brain (heart, muscle, kidney, liver and plasma) by between 50 and 80 %, depending on the tissue. This partial taurine depletion did not affect either basal synaptic transmission or the late phase of long-term potentiation (late-LTP) in hippocampal slices. In vivo microdialysis studies in the hippocampus revealed that GES treatment reduced extracellular taurine levels and the magnitude of taurine released in response to the application of either N-methyl-D-aspartate (NMDA) or a hypoosmotic solution, without affecting release mechanisms. Finally, we demonstrated in hippocampal slices that a brief GES application can mimic taurine action on the conversion of a decremental LTP into a perdurable late-LTP, concluding that GES might replace taurine function in some mechanisms such as those implicated in synaptic plasticity.

Taurine content in different brain structures during ageing: effect on hippocampal synaptic plasticity.

A reduction in taurine content accompanies the ageing process in many tissues. In fact, the decline of brain taurine levels has been associated with cognitive deficits whereas chronic administration of taurine seems to ameliorate age-related deficits such as memory acquisition and retention. In the present study, using rats of three age groups (young, adult and aged) we determined whether the content of taurine and other amino acids (glutamate, serine, glutamine, glycine, alanine and GABA) was altered during ageing in different brain areas (cerebellum, cortex and hippocampus) as well non-brain tissues (heart, kidney, liver and plasma). Moreover, using hippocampal slices we tested whether ageing affects synaptic function and plasticity. These parameters were also determined in aged rats fed with either taurine-devoid or taurine-supplemented diets. With age, we found heterogeneous changes in amino acid content depending on the amino acid type and the tissue. In the case of taurine, its content was reduced in the cerebellum of adult and aged rats, but it remained unchanged in the hippocampus, cortex, heart and liver. The synaptic response amplitude decreased in aged rats, although the late phase of long-term synaptic potentiation (late-LTP), a taurine-dependent process, was not altered. Our study highlights the stability of taurine content in the hippocampus during ageing regardless of whether taurine was present in the diet, which is consistent with the lack of changes detected in late-LTP. These results indicate that the beneficial effects of taurine supplementation might be independent of the replenishment of taurine stores.

Association of C4d deposition with clinical outcomes in IgA nephropathy.

BACKGROUND AND OBJECTIVES: Several studies have suggested that activation of the complement system is a contributing pathogenic mechanism in IgA nephropathy (IgAN). C4d staining is an inexpensive and easy-to-perform method for the analysis of renal biopsies. This study aimed to assess the clinical and prognostic implications of C4d staining in IgAN. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This retrospective cohort study included 283 patients with IgAN in 11 hospitals in Spain who underwent a renal biopsy between 1979 and 2010. The primary predictor was mesangial C4d staining. Secondary predictors included demographic, clinical, and laboratory characteristics, and Oxford pathologic classification criteria. The primary end point was the cumulative percentage of patients who developed ESRD, defined as onset of chronic dialysis or renal transplantation. C4d was analyzed by immunohistochemical staining using a polyclonal antibody. Kaplan-Meier and Cox proportional hazards analyses were performed to evaluate the effect of C4d staining on renal survival. RESULTS: There were 109 patients (38.5%) and 174 patients (61.5%) who were classified as C4d positive and C4d negative, respectively. Renal survival at 20 years was 28% in C4d-positive patients versus 85% in C4d-negative patients (P<0.001). Independent risk factors associated with ESRD were as follows: proteinuria (hazard ratio [HR] per every 1 g/d increase. 1.16; 95% confidence interval [95% CI], 1.03 to 1.31; P=0.01), eGFR (HR per every 1 ml/min per 1.73 m(2) increase, 0.96; 95% CI, 0.94 to 0.97; P<0.001), T2 Oxford classification (tubular atrophy/interstitial fibrosis, >50%; HR, 4.42; 95% CI, 1.40 to 13.88; P=0.01), and C4d-positive staining (HR, 2.45; 95% CI, 1.30 to 4.64; P=0.01). CONCLUSIONS: C4d-positive staining is an independent risk factor for the development of ESRD in IgAN. This finding is consistent with the possibility that complement activation is involved in the pathogenesis of this disease.

Modelo de intervención AFASINCA para familiares de niños con cáncer / AFASINCA intervention model for children's families with cancer

Resumen

La familia que vive la experiencia de un hijo con cáncer presenta una carga emocional y cambios importantes que requieren de la aceptación de tratamientos rigurosos, necesitan, reorganizar funciones propias del núcleo familiar, y sobre todo fortalecer las relaciones y valores; bajo esta perspectiva, la sociedad actualmente demanda mejor atención por parte del equipo de salud, con un sentid humanista. Por estas razones las enfermeras(os) tienen la responsabilidad de desarrollar conocimientos y habilidades aprendidos y proporcionar los cuidados con profesionalismo, mediante nuevas propuestas o modelos de cuidado. El objetivo principal de la familia, aún no está incorporado en la filosofía del sistema de atención pediátrica. El acercamiento a la familia con situación de un hijo o hija con cáncer es muy importante, entender sus cambios contextuales y reasegurar el ejercicio de la enfermería y la visión y prestigio de la institución por medio del Modelo de “Intervención para Afrontamiento de Familias en Situación de Niño con Cáncer” (AFASINCA).

Summary

The situation of a family in case of a son or daughter with cancer deals with an emotional load and important changes that require the acceptance of rigorous treatments, deal with important demands like material and emotional adjustments, reorganize functions, change roles, strengthen the relation and values; under this perspective, today’s society demand increasingly more and better care with a humanistic sense, in which the professional nurses should have the responsibility of developing knowledge and skills to promote their professionalism, through the creation of new proposals, guides and or ways of care. The main focus in the family is not yet incorporated in the philosophy of care within the pediatric health system. Family approach is very important in the situation of a son or daughter with cancer, understand their contextual changes and to reassure the professional exercises of nursing and the institutions vision through “the model of nursing intervention for the family coping in the situation of a son or daughter with cancer” in which I present in the annexed investigation, AFASINCA Model.

Involvement of the CA3-CA1 synapse in the acquisition of associative learning in behaving mice.

One of the brain sites more directly related with learning and memory processes is the hippocampus. We recorded, in conscious mice, the activity-dependent changes taking place at the hippocampal CA3-CA1 synapse during the acquisition, extinction, recall, and reconditioning of an associative task. Mice were classically conditioned to evoke eyelid responses using a trace [conditioned stimuli (CS), tone; unconditioned stimuli (US), shock] paradigm. A single electrical pulse presented to the Schaffer collateral-commissural pathway during the CS-US interval evoked a monosynaptic field EPSP (fEPSP) at ipsilateral CA1 pyramidal cells. The slope of evoked fEPSPs increased across conditioning sessions and decreased during extinction, being linearly related to learning evolution. In contrast, fEPSPs were not modified when evoked in control mice in the absence of a conditioning protocol. Long-term potentiation (LTP) evoked by high-frequency stimulation of Schaffer collaterals prevented acquisition, extinction, recall, or reconditioning, depending on the moment when it was triggered. Learning and memory impairments evoked by LTP induction resulted probably from the functional saturation of the CA3-CA1 synapse, although an additional disturbance of the subsequent information transfer toward postsynaptic circuits cannot be discarded. CGP 39551 [(E)-(+/-)-2-amino-4-methyl-5-phosphono-3-pentenoic acid ethyl ester] (an NMDA antagonist) prevented LTP induction in behaving mice, as well as the acquisition of an eyelid learned response, and the synaptic changes taking place at the CA3-CA1 synapse across conditioning. In conclusion, the responsivity of the CA3-CA1 synapse seems to be modulated during associative learning, and both processes are prevented by experimental LTP or NMDA-receptor inactivation. Our results provide evidence of a relationship between activity-dependent synaptic plasticity and associative learning in behaving mice.

Molecular mechanisms of the alterations in NMDA receptor-dependent long-term potentiation in hyperammonemia.

Long-term potentiation (LTP) is a long-lasting enhancement of synaptic transmission efficacy and is considered the base for some forms of learning and memory. Hyperammonemia impairs LTP in hippocampus. Proper LTP induction in hippocampal slices requires activation of the soluble guanylate cyclase (sGC)-protein kinase G (PKG)-cyclic guanosine monophosphate (cGMP)-degrading phosphodiesterase pathway. Hyperammonemia impairs LTP by impairing the tetanus-induced activation of this pathway. The tetanus induces a rapid cGMP rise, reaching a maximum at 10 s, both in the absence or in the presence of ammonia. The increase in cGMP is followed, in control slices, by a sustained decrease in cGMP because of PKG-mediated activation of cGMP-degrading phosphodiesterase, which is required for maintenance of LTP. Hyperammonemia prevents completely tetanus-induced decrease in cGMP by impairing PKG-mediated activation of cGMP-degrading phosphodiesterase. Addition of 8 Br-cGMP to slices treated with ammonia restores both phosphodiesterase activation and maintenance of LTP. Impairment of LTP in hyperammonemia may be involved in the impairment of the cognitive function in patients with hepatic encephalopathy.

Chronic hyperammonemia in vivo impairs long-term potentiation in hippocampus by altering activation of cyclic GMP-dependent-protein kinase and of phosphodiesterase 5.

Long-term potentiation (LTP) is impaired in the CA1 area of hippocampal slices from rats with chronic moderate hyperammonemia. We studied the mechanisms by which hyperammonemia in vivo impairs LTP. This process requires sequential activation of soluble guanylate cyclase, cyclic GMP-dependent protein kinase (PKG) and cyclic GMP-degrading phosphodiesterase. Application of the tetanus induced a rapid increase of cyclic GMP in slices from control or hyperammonemic rats, which is followed in control slices by a sustained decrease in cyclic GMP due to sustained activation of cyclic GMP-degrading phosphodiesterase, which in turn is due to sustained activation of PKG. In slices from rats with chronic hyperammonemia tetanus-induced decrease in cyclic GMP was delayed and transient due to lower and transient activation of PKG and of the phosphodiesterase. Hyperammonemia-induced impairment of LTP may be involved in the alterations of cognitive function in patients with hepatic encephalopathy.

Sequential activation of soluble guanylate cyclase, protein kinase G and cGMP-degrading phosphodiesterase is necessary for proper induction of long-term potentiation in CA1 of hippocampus. Alterations in hyperammonemia.

Long-term potentiation (LTP) is a long-lasting enhancement of synaptic transmission efficacy and is considered the base for some forms of learning and memory. Nitric oxide (NO)-induced formation of cGMP is involved in hippocampal LTP. We have studied in hippocampal slices the effects of application of a tetanus to induce LTP on cGMP metabolism and the mechanisms by which cGMP modulates LTP. Tetanus application induced a transient rise in cGMP, reaching a maximum at 10s and decreasing below basal levels 5 min after the tetanus, remaining below basal levels after 60 min. Soluble guanylate cyclase (sGC) activity increased 5 min after tetanus and returned to basal levels at 60 min. The decrease in cGMP was due to sustained tetanus-induced increase in cGMP-degrading phosphodiesterase activity, which remained activated 60 min after tetanus. Tetanus-induced activation of PDE and decrease of cGMP were prevented by inhibiting protein kinase G (PKG). This indicates that the initial increase in cGMP activates PKG that phosphorylates (and activates) cGMP-degrading PDE, which, in turn, degrades cGMP. Inhibition of sGC, of PKG or of cGMP-degrading phosphodiesterase impairs LTP, indicating that proper induction of LTP involves transient activation of sGC and increase in cGMP, followed by activation of cGMP-dependent protein kinase, which, in turn, activates cGMP-degrading phosphodiesterase, resulting in long-lasting reduction of cGMP content. Hyperammonemia is the main responsible for the neurological alterations found in liver disease and hepatic encephalopathy, including impaired intellectual function. Hyperammonemia impairs LTP in hippocampus by altering the modulation of this sGC-PKG-cGMP-degrading PDE pathway. Exposure of hippocampal slices to 1 mM ammonia completely prevents tetanus-induced decrease of cGMP by impairing PKG-mediated activation of cGMP-degrading phosphodiesterase. This impairment is responsible for the loss of the maintenance of LTP in hyperammonemia, and may be also involved in the cognitive impairment in patients with hyperammonemia and hepatic encephalopathy.

Hyperammonemia impairs long-term potentiation in hippocampus by altering the modulation of cGMP-degrading phosphodiesterase by protein kinase G.

Hyperammonemia impairs long-term potentiation (LTP) in hippocampus, by an unknown mechanism. LTP in hippocampal slices requires activation of the soluble guanylate cyclase (sGC)-protein kinase G (PKG)-cGMP-degrading phosphodiesterase pathway. The aim of this work was to assess whether hyperammonemia impairs LTP by impairing the tetanus-induced activation of this pathway. The tetanus induced a rapid cGMP rise, reaching a maximum at 10 s, both in the absence or presence of ammonia. The increase in cGMP is followed in control slices by a sustained decrease in cGMP due to PKG-mediated activation of cGMP-degrading phosphodiesterase, which is required for maintenance of LTP. Hyperammonemia prevents completely tetanus-induced cGMP decrease by impairing PKG-mediated activation of cGMP-degrading phosphodiesterase. Addition of 8Br-cGMP to slices treated with ammonia restores both phosphodiesterase activation and maintenance of LTP. Impairment of LTP in hyperammonemia may be involved in the impairment of the cognitive function in patients with hepatic encephalopathy.

Long-term potentiation in hippocampus involves sequential activation of soluble guanylate cyclase, cGMP-dependent protein kinase, and cGMP-degrading phosphodiesterase.

Previous studies indicate that cGMP is involved in long-term potentiation (LTP). However, the effects of application of tetanus to induce LTP on cGMP content and the mechanisms by which cGMP may modulate LTP have not been reported. The aim of this work was to study the time course of the changes in cGMP content and of the activity of soluble guanylate cyclase (sGC) (the enzyme that synthesizes cGMP) during LTP. Moreover, we also studied how the changes in cGMP affect cGMP-dependent protein kinase (PKG) and cGMP-degrading phosphodiesterase and the possible role of these changes in LTP. Application of tetanus induced a rise in cGMP, reaching a maximum 10 sec after tetanus. cGMP content decreased below basal levels 5 min after tetanus and remained decreased after 60 min. Activity of sGC increased 5 min after tetanus and returned to basal at 60 min. Tetanus increased the activity of cGMP-degrading phosphodiesterase at 5 and 60 min. GMP, the product of degradation, was increased at 5 and 60 min. Activation of phosphodiesterase and a decrease in cGMP were prevented by inhibiting PKG with Rp-8-bromoguanosine-cGMPS (Rp-8-Br-cGMPS). Inhibition of sGC [with ODQ (oxadiazolo quinoxalin-1-one) or NS 2028 (4H-8-bromo-1,2,4-oxadiazolo(3,4-d)benz(b)(1,4)oxazin-1-one)], of PKG (with Rp-8-Br-cGMPS), or of cGMP-degrading phosphodiesterase [with zaprinast or MBAM (4-[[3',4'-(methylenedioxy)benzyl]amino]-6-methoxyquinazoline) ] impairs LTP. The results indicate that induction of LTP involves transient activation of sGC and an increase in cGMP, followed by activation of cGMP-dependent protein kinase, which, in turn, activates cGMP-degrading phosphodiesterase, resulting in long-lasting reduction of cGMP content.

Effects of hyperammonemia and liver failure on glutamatergic neurotransmission.

Glutamate is the main excitatory neurotransmitter in mammals. Glutamatergic neurotransmission involves several steps, beginning with release of glutamate from the presynaptic neuron. Glutamate in the extracellular space activates glutamate receptors present in the synaptic membranes, leading to activation of signal transduction pathways associated with these receptors. To avoid continuous activation of glutamate receptors, glutamate is removed from the synaptic cleft by specific glutamate transporters located mainly on astrocytes. All these steps are tightly modulated under physiological conditions, and alterations of any of the above steps may result in impairment of glutamatergic neurotransmission, leading to neurological alterations. There are studies in the literature reporting alterations in all these steps in hyperammonemia and/or hepatic failure. Glutamatergic neurotransmission modulates important cerebral processes. Some of these processes are altered in patients with liver disease and hepatic encephalopathy, who show altered sleep-wake patterns, neuromuscular coordination, and decreased intellectual capacity. The alterations in glutamatergic neurotransmission may be responsible for some of these neurological alterations found in hepatic encephalopathy. The effects of hyperammonemia and liver failure on different steps of glutamatergic neurotransmission including alterations of glutamate concentration in the extracellular fluid in brain, transport and transporters of glutamate, the content and function of different types of glutamate receptors and signal transduction pathways. Alterations induced by hyperammonemia and liver failure on the glutamate-nitric oxide-cGMP pathway in brain may result in changes in long-term potetiation and learning ability.

Proyecto Salud Adolescente Pilar (SAP) / Pilar project health teenager

royecto de Salud del Adolescente en la ciudad de Pilar, que tiene como objetivo disminuir la incidencia de embarazo adolescente a tráves de un proceso de IEC (Información, Educación y Comunicación) y la implementación de un servicio de salud diferenciado en el Hospital Regional de Pilar, esta estrategia de IEC se constituye en un instrumento de sensibilización y activación de la opinión pública capaz de producir cambios conductuctuales - actiduales y desarrollar conductas sexuales y reproductivas saludables en los y las adolescente de cinco barrios del distrito de Pilar capital departamental con mayor concentración poblacional

Proyecto de intervención: programa de capacitación en reanimación cardiopulmonar básica para familiares de personas en riesgo de sufrir paro cardiorespiratorio / Project of participation: training program in basic cardiopulmonary resuscitation for the family of people with cardiorespiratory risk

El siguiente programa educativo tiene por objetivo capacitar en Reanimación Cardiopulmonar (RCP) básica a familiares de pacientes que hayan estado hospitalizados en la Unidad Coronaria del Hospital Clínico de la Universidad Católica (PUC) y que se encuentren en riesgo de sufrir paro cardiorespiratorio, lo que les permitirá enfrentar una situación de emergencia, pudiendo entregar un soporte vital básico hasta que llegue la ayuda avanzada. El Programa de Capacitación se aplicó en dos sesiones en que asistieron un total de 16 personas adultas de ambos sexos. Consta de una parte teórica en que se entregan los principales contenidos, previo a lo cual se realiza una evaluación de los conocimientos que poseen las personas que se capacitarán, y una segunda parte que consiste en la práctica de lo aprendido. Los medios audiovisuales utilizados se crearon pensando en las características de aprendizaje que poseen los adultos. Los contenidos y la metodología fueron evaluados mediante un test al final de la sesión educativa, como un modo de objetivar el resultado de la capacitación a corto plazo. La finalidad de esta tesis, es crear un programa de capacitación para familiares de personas que poseen riesgo de sufrir un PCR, para que sea implementado en la Unidad Coronaria del Hospital Clínico de PUC como parte de la educación que entregan las enfermeras de esta unidad