Numerical analysis of aerodynamic performance of the Ram Air Turbine in an aircraft.

A rotor design of a Ram Air Turbine (RAT) for a commercial aircraft was created taking three sections with different airfoils along the blade; those sections were assessed to evaluate their performance at different critical velocities (41, 81 and 251 m/s) and choose the best profile configuration generating a new proposal to increase the glide ratio by reducing the drag, which is helpful in emergency cases. The Blade Element Momentum (BEM) theory and Computational Fluid Dynamics (CFD) were used to analyze an initial design, then validating these results with the open software QBlade. For the BEM theory a program was created for the design and performance of the RAT adding the Viterna methodology for airfoil analysis. 16 designs were proposed by strategically interchanging wing profiles in different blade sections. These designs were analyzed by CFD, using the complete rotor and the S S T k - ω turbulence model. An optimal geometry was found, presenting a significant drag reduction of 25% generating an increase in the glide ratio and improving aircraft control in addition to maintaining the power generation above the desired values; therefore, it recommends using different airfoils for each section of a RAT's rotor blade.

Prolactin prevents the kainic acid-induced neuronal loss in the rat hippocampus by inducing prolactin receptor and putatively increasing the VGLUT1 overexpression.

Neuroprotective effects of short prolactin (PRL) pre-treatment against kainic acid (KA)-induced damage include neuron loss avoidance in all hippocampal regions and attenuation of seizures. Recent evidence points PRL receptor (PRL-R) as mediator of such neuroprotective effects and seizures as regulators of neuronal marker transcript expression in the hippocampus. Here, we investigated if a daily PRL dose of 100 µg or vehicle for 14 days in ovariectomized rats (OVX) prevents neuron loss induced by KA administered on the third day of PRL treatment in a systemic single dose of 7.5 mg/kg or vehicle, and promotes PRL-R, vesicular glutamate transporter 1 (VGLUT1) and glutamic acid decarboxylase 65 (GAD65) expression changes in the hippocampus of sacrificed rats 27 days after the KA administration. Immunostaining for Neu-N and PRL-R revealed significant neuron number and PRL-R expression reduction induced by KA that was prevented and turned into overexpression respectively in all hippocampal regions when PRL was added; while VGLUT1,and GAD65 immunostaining displayed expression decrease in the CA1 of injured rats, prevented in the last case and turned into VGLUT1, overexpression when administered PRL. These data indicate that chronic PRL administration before damage induces hippocampal neuroprotection associated with PRL-R and VGLUT1 overexpression, the latter in a regiondependent way.

An enriched environment and 17-beta estradiol produce similar pro-cognitive effects on ovariectomized rats.

Estrogen depletion due to aging, surgery or pathological events can cause a multitude of problems, including neurodegenerative alterations. In rodents without ovaries, 17-beta estradiol (E2) has been shown to produce beneficial effects on cognition, stimulating brain regions (e.g., the neocortex, hippocampus and amygdala) related to cognition and learning. Another treatment that stimulates these brain regions is an enriched environment (EE), which is a complex set of external factors in the immediate surroundings that facilitates greater stimulation of sensorial, cognitive and motor circuits of the brain. The aim of the present study was to test, using an animal model of ovariectomy-induced impairment of memory, the relative effect of E2 (with a time-released pellet; 1 µg/rat/day), EE exposure and a combination of both treatments. Experimental and control groups were submitted to two memory tests 18 weeks post-surgery: the autoshaping learning task (ALT) for measuring associative learning and the novel object recognition test (NORT) for evaluating short- and long-term memory. To assess potential motor impairments caused by treatments, all rats were tested after the ALT in an automatic activity counter. Results from ALT show that the ovariectomy blocked the conditioned responses displayed, an effect rescued by chronic treatment with estrogen or EE exposure. The combination of both treatments did not improve the results obtained separately. In the NORT, the exploration time for recognizing a novel object was similar in the short run with all groups, but greater in the long run with hormone administration or EE exposure. As with the ALT, in the NORT there was no improvement shown by the combination treatment. These data were not masked by changes in spontaneous activity because this parameter was not modified in the rats by either treatment. Possible action mechanisms are proposed, taking into account the role of corticosterone and BDNF on cognition.