Mixed shock in patients with acute myocardial infarction: Nursing interventions. / Shock mixto en paciente con infarto agudo de miocardio: intervenciones enfermeras.

INTRODUCTION AND OBJECTIVES: We present a clinical case of a 40-year-old woman diagnosed with acute myocardial infarction (AMI) in Killip I who was admitted to our hospital. She experienced complications in the haemodynamic lab and in the operating room, including cardiogenic and anaphylactic shock requiring ventricular assist support. Conservative management support with inotropes and vasopressors in cardiogenic shock has been shown to be insufficient in many patients to maintain adequate perfusion and prevent irreversible multiple organ dysfunction syndrome. For this reason, short-term mechanical circulatory support systems are increasing substantially. The objective of this article is to develop optimal and individualised care plans using the NANDA, NOC, NIC taxonomies. CLINICAL OBSERVATION: An evaluation based on Virginia Hendersons basic needs was made, and two altered needs stood out: breathing and circulation. The patient required mechanical ventilation and mechanical circulatory support. INTERVENTIONS: In relation to the highlighted needs, six diagnoses were prioritized according to the NANDA taxonomy using the Análisis de Resultado del Estado Actual (AREA) (Outcome-Present State Test (OPT)) model: risk of decreased cardiac output, impaired spontaneous ventilation, impaired tissue integrity, risk of disuse syndrome, risk of infection and risk of hypothermia. DISCUSSION AND CONCLUSIONS: Outcome criteria scores showed a favourable evolution after 96h. The development of a standardized NANDA-NOC-NIC language allowed us to organize the nursing care plan.

Mixed shock in patients with acute myocardial infarction: Nursing interventions.

INTRODUCTION AND OBJECTIVES: We present a clinical case of a 40-year-old woman diagnosed with acute myocardial infarction (AMI) in Killip I who was admitted to our hospital. She experienced complications in the haemodynamic lab and in the operating room, including cardiogenic and anaphylactic shock requiring ventricular assist support. Conservative management support with inotropes and vasopressors in cardiogenic shock has been shown to be insufficient in many patients to maintain adequate perfusion and prevent irreversible multiple organ dysfunction syndrome. For this reason, short-term mechanical circulatory support systems are increasing substantially. The objective of this article is to develop optimal and individualised care plans using the NANDA, NOC, NIC taxonomies. CLINICAL OBSERVATION: An evaluation based on Virginia Henderson's basic needs was made, and two altered needs stood out: breathing and circulation. The patient required mechanical ventilation and mechanical circulatory support. INTERVENTIONS: In relation to the highlighted needs, six diagnoses were prioritized according to the NANDA taxonomy using the Análisis de Resultado del Estado Actual (AREA) (Outcome-Present State Test (OPT)) model: risk of decreased cardiac output, impaired spontaneous ventilation, impaired tissue integrity, risk of disuse syndrome, risk of infection and risk of hypothermia. DISCUSSION AND CONCLUSIONS: Outcome criteria scores showed a favourable evolution after 96 h. The development of a standardized NANDA-NOC-NIC language allowed us to organize the nursing care plan.

The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines.

Copy number variation (CNV) at the 15q11.2 region has been identified as a significant risk locus for neurological and neuropsychiatric conditions such as schizophrenia (SCZ) and autism spectrum disorder (ASD). However, the individual roles for genes at this locus in nervous system development, function and connectivity remain poorly understood. Haploinsufficiency of one gene in this region, Cyfip1, may provide a model for 15q11.2 CNV-associated neuropsychiatric phenotypes. Here we show that altering CYFIP1 expression levels in neurons both in vitro and in vivo influences dendritic complexity, spine morphology, spine actin dynamics and synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor lateral diffusion. CYFIP1 is highly enriched at synapses and its overexpression in vitro leads to increased dendritic complexity. Neurons derived from Cyfip1 heterozygous animals on the other hand, possess reduced dendritic complexity, increased mobile F-actin and enhanced GluA2-containing AMPA receptor mobility at synapses. Interestingly, Cyfip1 overexpression or haploinsufficiency increased immature spine number, whereas activity-dependent changes in spine volume were occluded in Cyfip1 haploinsufficient neurons. In vivo, Cyfip1 heterozygous animals exhibited deficits in dendritic complexity as well as an altered ratio of immature-to-mature spines in hippocampal CA1 neurons. In summary, we provide evidence that dysregulation of CYFIP1 expression levels leads to pathological changes in CNS maturation and neuronal connectivity, both of which may contribute to the development of the neurological symptoms seen in ASD and SCZ.

The Armc10/SVH gene: genome context, regulation of mitochondrial dynamics and protection against Aß-induced mitochondrial fragmentation.

Mitochondrial function and dynamics are essential for neurotransmission, neural function and neuronal viability. Recently, we showed that the eutherian-specific Armcx gene cluster (Armcx1-6 genes), located in the X chromosome, encodes for a new family of proteins that localise to mitochondria, regulating mitochondrial trafficking. The Armcx gene cluster evolved by retrotransposition of the Armc10 gene mRNA, which is present in all vertebrates and is considered to be the ancestor gene. Here we investigate the genomic organisation, mitochondrial functions and putative neuroprotective role of the Armc10 ancestor gene. The genomic context of the Armc10 locus shows considerable syntenic conservation among vertebrates, and sequence comparisons and CHIP-data suggest the presence of at least three conserved enhancers. We also show that the Armc10 protein localises to mitochondria and that it is highly expressed in the brain. Furthermore, we show that Armc10 levels regulate mitochondrial trafficking in neurons, but not mitochondrial aggregation, by controlling the number of moving mitochondria. We further demonstrate that the Armc10 protein interacts with the KIF5/Miro1-2/Trak2 trafficking complex. Finally, we show that overexpression of Armc10 in neurons prevents Aß-induced mitochondrial fission and neuronal death. Our data suggest both conserved and differential roles of the Armc10/Armcx gene family in regulating mitochondrial dynamics in neurons, and underscore a protective effect of the Armc10 gene against Aß-induced toxicity. Overall, our findings support a further degree of regulation of mitochondrial dynamics in the brain of more evolved mammals.