Does postoperative orbital volume predict postoperative globe malposition after blow-out fracture reconstruction? A 6-month clinical follow-up study

PurposeThe aim of this study was to investigate the relationship between intraorbital volume change caused by orbital fracture and globe malposition (GMP) in blow-out fracture patients undergoing surgery and to clarify the significance of different radiologically detected predictors associated with GMP.Patients and methodsA 6-month prospective follow-up study of unilateral isolated orbital fractures was designed and implemented. The main outcome variable was GMP (present or absent); the secondary outcome was orientation of GMP (horizontal or vertical). The primary predictor variable was postoperative orbital volume difference determined as the difference between the fractured and non-fractured orbit (measured in milliliter and analyzed in milliliter and percentages). The explanatory variables were gender, age, treatment delay from trauma to surgery, fracture site, horizontal depth of the fracture, fracture area, maximum vertical dislocation of the fracture, and preoperative volume difference.ResultsA total of 15 patients fulfilled the inclusion criteria and were followed for 6months from a larger cohort. GMP was detected in 6/15 patients (40.0%). GMP was more often present in large (2.5cm(2)) fractures (55.6%), in combined orbital fractures (50.0%), and in fractures with preoperative volume difference 2.5ml (62.5%) regardless of the postoperative volume correction. Postoperatively, patients with and without GMP displayed overcorrection of orbital volume; 4.15% corresponded to 1.15ml (with GMP) and 7.6% corresponded to 1.9ml (without GMP).ConclusionGMP was present in large and combined orbital fractures. Clinically detectable postoperative GMP occurred despite satisfactory orbital reconstruction and overcorrection. Mild GMP, however, is not significant for the patient.Peer reviewe

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

BACKGROUND: To better understand the complex molecular level interactions seen in the pathogenesis of Alzheimer's disease, the results of the wet-lab and clinical studies can be complemented by mathematical models. Astrocytes are known to become reactive in Alzheimer's disease and their ionic equilibrium can be disturbed by interaction of the released and accumulated transmitters, such as serotonin, and peptides, including amyloid- peptides (A). We have here studied the effects of small amounts of A25-35 fragments on the transmitter-induced calcium signals in astrocytes by Fura-2AM fluorescence measurements and running simulations of the detected calcium signals. METHODOLOGY/PRINCIPAL FINDINGS: Intracellular calcium signals were measured in cultured rat cortical astrocytes following additions of serotonin and glutamate, or either of these transmitters together with A25-35. A25-35 increased the number of astrocytes responding to glutamate and exceedingly increased the magnitude of the serotonin-induced calcium signals. In addition to A25-35-induced effects, the contribution of intracellular calcium stores to calcium signaling was tested. When using higher stimulus frequency, the subsequent calcium peaks after the initial peak were of lower amplitude. This may indicate inadequate filling of the intracellular calcium stores between the stimuli. In order to reproduce the experimental findings, a stochastic computational model was introduced. The model takes into account the major mechanisms known to be involved in calcium signaling in astrocytes. Model simulations confirm the principal experimental findings and show the variability typical for experimental measurements. CONCLUSIONS/SIGNIFICANCE: Nanomolar A25-35 alone does not cause persistent change in the basal level of calcium in astrocytes. However, even small amounts of A25-35, together with transmitters, can have substantial synergistic effects on intracellular calcium signals. Computational modeling further helps in understanding the mechanisms associated with intracellular calcium oscillations. Modeling the mechanisms is important, as astrocytes have an essential role in regulating the neuronal microenvironment of the central nervous system

Bidirectional Coupling between Astrocytes and Neurons Mediates Learning and Dynamic Coordination in the Brain: A Multiple Modeling Approach

In recent years research suggests that astrocyte networks, in addition to nutrient and waste processing functions, regulate both structural and synaptic plasticity. To understand the biological mechanisms that underpin such plasticity requires the development of cell level models that capture the mutual interaction between astrocytes and neurons. This paper presents a detailed model of bidirectional signaling between astrocytes and neurons (the astrocyte-neuron model or AN model) which yields new insights into the computational role of astrocyte-neuronal coupling. From a set of modeling studies we demonstrate two significant findings. Firstly, that spatial signaling via astrocytes can relay a “learning signal” to remote synaptic sites. Results show that slow inward currents cause synchronized postsynaptic activity in remote neurons and subsequently allow Spike-Timing-Dependent Plasticity based learning to occur at the associated synapses. Secondly, that bidirectional communication between neurons and astrocytes underpins dynamic coordination between neuron clusters. Although our composite AN model is presently applied to simplified neural structures and limited to coordination between localized neurons, the principle (which embodies structural, functional and dynamic complexity), and the modeling strategy may be extended to coordination among remote neuron clusters