Characteristics of the G-loads in sports stunt flying

Thirty well-qualified flying sportsmen, aged 22-42, who performer 210 aerobatic flights onboard a sporting airplane Yak-50, were examined, using an automatic monitoring system. The flyers were exposed to +9 Gz and -6 Gz as a maximum the duration of which was 10 s and 5 s, respectively. The onset rate varied from 0.5 to 2.5 G/s (with the mean rate 1 G/s), reaching 4.2 G/s as a maximum. On the average, the training flight lasts 25 min, 45-50% of which the pilot experiences acceleration of various values and different sign. The most common acceleration values are: +6 and +7 Gz or -4 and -5 Gz.     

Locomotor effects of nitrous oxide in mice: requirement of newly-synthesized and main intraneuronal storage pools of dopamine

Abstract— Nitrous oxide increases locomotor activity in mice. Other locomotor stimulants are thought to act via central dopaminergic mechanisms and can be divided into two groups as determined by their antagonism by tyrosine hydroxylase inhibitors or by reserpine pretreatment. The purpose of the present study was to determine if nitrous oxide fits one or the other of the groups. Mice were acclimatized for 1 h to exposure chambers (4 L filtration flasks), in air, delivered at 4 L min^?1 and then exposed to N₂O:O₂ (50:50), also delivered at 4 L min^?1. Locomotor activity was evaluated at 10 min intervals throughout the experiment. Racemic α-methyltyrosine methyl ester HCl (200 mg kg^?1), administered at the beginning of acclimatization, almost totally eliminated the nitrous oxide effect but not that of methylphenidate HCl (20 mg kg^?1). Reserpine pretreatment (5 mg kg^?1 18 h) totally eliminated the nitrous oxide effect but not that of amphetamine (5 mg kg^?1). The results suggest that nitrous oxide requires both the newly synthesized and the main storage pools of dopamine and do not allow assignment of the agent, specifically, to either of the groups.     

Low back pain: conservative treatment with artificial shock absorbers

A new method of conservative treatment for low back pain (LBP) was studied by follow-up investigation of 382 patients during the last five years. The attempt to reduce repetitive impulsive intervertebral impact in the troublesome S1-L5-4 area by significant improvement of the foot's attenuational capacity through artificial viscoelastic shock absorbing was prompted by the authors' work on decreased capability of LBP spines to attenuate axially propagated walking stresses. Viscoelastic shoe inserts were used in addition to light flexible shoes as artificial shock absorbing devices. Maximal amplitudes of bone oscillation during walking were reduced by about 40% by the viscoelastic inserts. Rapid and surprisingly significant improvement of pain syndrome and patient mobility occurred in about 80% of the patients. The accelerographic patterns recorded on a sacrum of patient with LBP were unusual for a healthy subject; they usually disappeared after treatment in LBP cases. Results suggested that poor walking impact attenuation was a true cause for prolonging intervertebral structures overstrain and consequent degeneration. It seemed logical that as spine damage could be explained primarily by prolonged impulsive overstrain, treatment must include viscoelastic inserts which increase foot shock absorbing capacity and help cushion the spine.     

Intrinsic factor-mediated absorption of cobalamin by guinea pig ileal cells

To investigate the fate of intrinsic factor and cobalamin during cobalamin absorption, we incubated enterocytes isolated from guinea pig ileum for periods of up to 30 min with ⁵⁷Co-labeled cyano-cobalamin bound either to human intrinsic factor or to rabbit intrinsic factor biosynthetically labeled with [³⁵S]methionine. When the labeled complex was incubated for 30 min with isolated ileal cells under conditions that block cellular metabolism, virtually all cellular radioactivity could be removed by washing the cell surface with EDTA or acid. In contrast, washing removed only half the radioactivity from cells incubated at 37°C in O₂. When residual cellular radioactivity was extracted and analyzed by gel filtration, 80-94% of both the ³⁵S and ⁵⁷Co radioactivity eluted in the same fractions as the original complex. The remaining 6-20% eluted as free [⁵⁷Co]cobalamin or [³⁵S]methionine. To examine events occurring after 30 min, we instilled into tied-off ileal loops of intact guinea pigs radiolabeled intrinsic factor-cobalamin complex and extracted nondissociable radioactivity 2-4.5 h later. The proportion of extracted ⁵⁷Co eluting as free cobalamin increased to 39-46%, that eluting as intrinsic factor-cobalamin complex declined to 22-45%, and 9-34% now eluted as a macromolecule that reacted with antitranscobalamin II antibody but not antiintrinsic factor antibody. Extracted ³⁵S radioactivity eluted in several peaks in addition to the intrinsic factor peak. These findings suggest that (a) after reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent process prevents removal of the complex from the cell surface by EDTA or acid; (b) cobalamin dissociates from intrinsic factor and, as suggested by previous workers, binds to a molecule antigenically similar to transcobalamin II; and (c) intrinsic factor is slowly degraded and forms breakdown products that are detectable in ileal extracts.