Numerical simulation of aerodynamic interference between ejected payload and the parent aircraft

The purpose of this paper is to develop reliable methodology for numerical modeling of the interference between parent aircraft and ejectable payload and to investigate the influence of the interference on aerodynamic characteristics of the payload. An appropriate algorithm for the said problem is proposed. A mathematical model for supersonic flow around a solid body as well as its finite volume discretization process is described. In the presented mathematical model, a turbulence model is added to the Navier-Stokes system of equations. Namely, Menter’s SST model was chosen. Coupled solver algorithm is reviewed. Implicit Euler scheme is used for time discretization and Newton’s method is implemented to linearize the system of equations. The specifics of determining the appropriate boundary conditions and nondimensionalization of the aerodynamic coefficients are described. The calculations for the isolated payload were performed on an unstructured grid with 9 million cells and for the payload interfered by the parent aircraft - on a 24 million grid. As a result, the summarized aerodynamic characteristics for the payload were obtained for the isolated payload as well as for the payload in presence of the parent aircraft. The characteristics of the isolated object are compared with the ones of the object in presence of the parent aircraft in two different positions - Y rel = 0 m and Y rel = 0.6 m. The developed method was verified using wind tunnel data. It was identified that in presence of the parent aircraft, the coefficients of normal and side force are not zero as opposed to the isolated payload. Moving away from the parent aircraft decreases the interference and thus the side force, as well as the pitch and yaw torques. The obtained results show that the proposed method could be used in other cases of aerodynamic interference between moving objects

DNA barcoding of the fishes of the genus <i>Alburnoides</i> (Actinopterygii, Cyprinidae) from Caucasus

<p>Spirlins of the genus <i>Alburnoides</i> are widespread fishes, which taxonomy has been rapidly developing in recent years. Mitochondrial cytochrome c oxidase subunit I (COI) was used as DNA barcode marker to create a reference dataset of Caucasian <i>Alburnoides</i> and to test its barcoding efficiency. All four previously known Caucasian species of <i>Alburnoides</i> were confirmed as valid species with high genetic distances to sister species as well confirmed as Caucasian endemics. <i>Alburnoides samiii,</i> previously known from Sefidroud basin (Iran), was discovered in Transcaucasia. The accuracy of species identification of Ponto-Caspian <i>Alburnoides</i> by DNA barcodes was 100%. In addition, one potentially new species within <i>A. gmelini</i> was revealed. Despite the limited ability of COI to infer phylogenetic relationships, study provided evidence that Ponto-Caspian lineage of <i>Alburnoides</i> includes significantly larger number of species from Caspian Sea basin and inland basins of Central Asia.</p

Unveiling the Link: Exploring Mitochondrial Dysfunction as a Probable Mechanism of Hepatic Damage in Post-Traumatic Stress Syndrome

PTSD is associated with disturbed hepatic morphology and metabolism. Neuronal mitochondrial dysfunction is considered a subcellular determinant of PTSD, but a link between hepatic mitochondrial dysfunction and hepatic damage in PTSD has not been demonstrated. Thus, the effects of experimental PTSD on the livers of high anxiety (HA) and low anxiety (LA) rats were compared, and mitochondrial determinants underlying the difference in their hepatic damage were investigated. Rats were exposed to predator stress for 10 days. Then, 14 days post-stress, the rats were evaluated with an elevated plus maze and assigned to HA and LA groups according to their anxiety index. Experimental PTSD caused dystrophic changes in hepatocytes of HA rats and hepatocellular damage evident by increased plasma ALT and AST activities. Mitochondrial dysfunction was evident as a predominance of small-size mitochondria in HA rats, which was positively correlated with anxiety index, activities of plasma transaminases, hepatic lipids, and negatively correlated with hepatic glycogen. In contrast, LA rats had a predominance of medium-sized mitochondria. Thus, we show links between mitochondrial dysfunction, hepatic damage, and heightened anxiety in PTSD rats. These results will provide a foundation for future research on the role of hepatic dysfunction in PTSD pathogenesis