Plasma Leak From the Circulation Contributes to Poor Outcomes for Preterm Infants: A Working Hypothesis

Preterm infants are at high risk of death and disability resulting from brain injury. Impaired cardiovascular function leading to poor cerebral oxygenation is a significant contributor to these adverse outcomes, but current therapeutic approaches have failed to improve outcome. We have re-examined existing evidence regarding hypovolemia and have concluded that in the preterm infant loss of plasma from the circulation results in hypovolemia; and that this is a significant driver of cardiovascular instability and thus poor cerebral oxygenation. High capillary permeability, altered hydrostatic and oncotic pressure gradients, and reduced lymphatic return all combine to increase net loss of plasma from the circulation at the capillary. Evidence is presented that early hypovolemia occurs in preterm infants, and that capillary permeability and pressure gradients all change in a way that promotes rapid plasma loss at the capillary. Impaired lymph flow, inflammation and some current treatment strategies may further exacerbate this plasma loss. A framework for testing this hypothesis is presented. Understanding these mechanisms opens the way to novel treatment strategies to support cardiovascular function and cerebral oxygenation, to replace current therapies, which have been shown not to change outcomes.

A Model Analysis of the MAVEN/ROSE Electron Density Profiles at Mars

<p>The electron density (N<sub>e</sub>) profiles over the northern high-latitude region measured with Radio Occultation Science Experiments (ROSE) onboard the Mars Atmosphere and Volatile Evolution (MAVEN) have indicated more complicated ionospheric structure of Mars than previously thought.  Some of the profiles have shown wide and narrow shapes of the main N<sub>e</sub> peaks, while others show anomalous characteristics of the topside plasma distribution.  Large variations in the topside N<sub>e</sub> scale heights are observed presumably in response to the outward flow of ionospheric plasma or changes in plasma temperatures.   We use our 1-D chemical diffusive model coupled with the Mars - Global Ionosphere Thermosphere Model (M-GITM) to interpret these N<sub>e</sub> profiles.  Our model is a coupled finite difference primitive equation model which solves for plasma densities and vertical ion fluxes.  The photochemical equilibrium in the model for each ion is assumed at the lower boundary, while the flux boundary condition is assumed at the upper boundary to simulate plasma loss from the Martian ionosphere.  The crustal magnetic field at the measured N<sub>e</sub> locations is weak and mainly horizontal and does not allow plasma to move vertically.   Thus, the primary plasma loss from the topside ionosphere at these locations is most likely caused by diverging horizontal fluxes of ions, indicating that the dynamics of the upper ionosphere of Mars is controlled by the solar wind.  The primary source of ionization in the model is due to solar EUV radiation.  We find that the variation in the topside N<sub>e</sub> scale heights is sensitive to magnitudes of upward ion fluxes derived from ion velocities that we impose at the upper boundary to explain the topside ionospheric structure.  The model requires upward velocities ranging from 60 ms<sup>-1</sup> to 80 ms<sup>-1</sup> for all ions to ensure an agreement with the measured N<sub>e</sub> profiles. The corresponding outward fluxes in the range 1.6 x 10<sup>6 </sup>– 3.8 x 10<sup>6</sup> cm<sup>-2</sup> s<sup>-1 </sup>are calculated for O<sub>2</sub><sup>+</sup> compared to those for O<sup>+</sup> in the range 4 x 105 – 6 x 105 cm<sup>-2</sup> s<sup>-1</sup>.  The model results for the northern N<sub>e</sub> profiles will be presented in comparison with the measured N<sub>e</sub> profiles.  This work is supported by Mohammed Bin Rashid Space Centre (MBRSC), Dubai, UAE, under Grant ID number 201604.MA.AUS.</p>

Pathogenetic factors of trauma and post-traumatic immunodeficiency

It is well known that the severe condition of patients can be caused not only by shock, but either by epiphenomenon of post-traumatick shock, mestly pulmonary, quite often ending by death, as a manifestation of a successful treatment- resistant secondary post-traumatic immunodeficiency. On our deep persuasion, based on the analysis of literature, and afterwards own experimental data, pathogeny of post-traumaticimmunodeficit at the level of organism and according to its pathogenetic prophylaxis can not be unsealed without the analysis of reaction of the immune system on the pathogenetic factors of trauma: 1) inadequate (foremost pain) impulsation from the damaged fabrics; 2) blood-plasma loss 3) entering blood of bioactive substances; 4) hypoxia. What are the immunomodulatory effects of these factors, not at all, but in case of specific mechanical injury? What is the specific contribution of each factors to the development of immunosuppression in case of specific injury, which one is the main pathogenetic factor in the pathogenesis of post-traumatic immunodeficiency? There are no publications about the specific role of known pathogenetic factors of trauma in the formation of post-traumatic immunodeficiency. The available data gives an idea about the role of pain afferentation, stress, blood loss, toxemia, hypoxia in modulating the immune response in general, regardless of any type of trauma, and the primary changes in the immune system of patients after assistance, including surgical intervention bearing the risk of developing immunosuppression along with drug therapy. The study of these problematic issues of the pathogenesis of post-traumatic immunodeficiency at the system level in the context of severe mechanical trauma experimental model is provided with sufficient understanding of significance of urgent and adequate assistance in the context of ideas about the role of pathogenetic factors of trauma in the pathogenesis of post-traumatic immunodeficiency.

Comparative study of photo-produced ionosphere in the close environment of comets

Context. The Giotto and Rosetta missions gave us the unique opportunity of probing the close environment of cometary ionospheres of 1P/Halley (1P) and 67P/Churyumov-Gerasimenko (67P). The plasma conditions encountered at these two comets were very different from each other, which mainly stem from the different heliocentric distances, which drive photoionization rates, and from the outgassing activities, which drive the neutral densities. Aims. We asses the relative contribution of different plasma processes that are ongoing in the inner coma: photoionization, transport, photoabsorption, and electron–ion dissociative recombination. The main goal is to identify which processes are at play to then quantitatively assess the ionospheric density. Methods. We provide a set of analytical formulas to describe the ionospheric number density profile for cometary environments that take into account some of these processes. We discuss the validity of each model in the context of the Rosetta and Giotto missions. Results. We show that transport is the dominant loss process at large cometocentric distances and low outgassing rates. Chemical plasma loss through e−-ion dissociative recombination matters around 67P near perihelion and at 1P during the Giotto flyby: its effects increase as the heliocentric distance decreases, that is, at higher outgassing activity and higher photoionization frequency. Photoabsorption is of importance for outgassing rates higher than 1028 s−1 and only close to the cometary nucleus, well below the location of both spacecraft. Finally, regardless of the processes we considered, the ion number density profile always follows a 1∕r law at large cometocentric distances.

Mathematical Model for Reducing the Concentration of a Chemical Substance Applicable in the Procedures of Plasmatic Treatment

The objective was to study the correlation between the mathematical form of a chemical that we want to lower its initial concentration by the regressive method and the purging of the body�s toxic present chemicals that need to be eliminated. We developed a chemical model, by which, to a given volume, with a certain (X - concentration %) dissolved substance in a container, the initial solvent, without solvit, is added (concentration 0%) with an equal rhythm to the one that is lost from the used container. The solution that will be lost will contain less and less concentrations of solvit, compared to the initial value X%. At the same time, the concentration of our chemical model will decrease. We applied a regressive mathematical formula to this model in order to calculate the concentration in the container in each moment. At the same time, we conducted treatment sessions in patients in which certain substances need to be eliminated, a procedure that complies with the described chemical model. We have demonstrated that at the same volume of 0% solvit wash, the substance purging with X% concentration is more effective, if the procedure starts with an initial loss of concentrated substance, with ulterior volume replacement. Laboratory data confirms the mathematical model in patients who started the procedure with plasma loss. The developed chemical model demonstrates that the initial loss of substance, hastens the decrease of the initial concentration, especially as the loss is higher at the beginning of the procedure if we use the same replacement volume without the substance in the initial solution. This model can be applied in plasma treatment methods in order to study the patient�s safety and the amount of plasma the patient can lose at the beginning.