Prevalence, Predictors & Prevention of Motion Sickness in Zero-G Parabolic Flights

INTRODUCTION Zero-G parabolic flight reproduces the weightlessness of space for short periods of time. However motion sickness may affect some fliers. The aim was to assess the extent of this problem and to find possible predictors and modifying factors. METHODS Airbus Zero-G flights consist of 31 parabolas performed in blocks. Each parabola consisted of 20s 0g sandwiched by 20s hypergravity of 1.5-1.8g. The survey covered n=246 person-flights (193 Males 53 Females), aged (M+/-SD) 36.0+/-11.3 years. An anonymous questionnaire included motion sickness rating (1=OK to 6=Vomiting), Motion Sickness Susceptibility Questionnaire (MSSQ), anti-motion sickness medication, prior Zero-G experience, anxiety level, and other characteristics. RESULTS Participants had lower MSSQ percentile scores 27.4+/-28.0 than the population norm of 50. Motion sickness was experienced by 33% and 12% vomited. Less motion sickness was predicted by older age, greater prior Zero-G flight experience, medication with scopolamine, lower MSSQ scores, but not gender nor anxiety. Sickness ratings in fliers pre-treated with scopolamine (1.81+/-1.58) were lower than for non-medicated fliers (2.93+/-2.16), and incidence of vomiting in fliers using scopolamine treatment was reduced by half to a third. Possible confounding factors including age, sex, flight experience, MSSQ, could not account for this. CONCLUSION Motion sickness affected one third of Zero-G fliers, despite being intrinsically less motion sickness susceptible compared to the general population. Susceptible individuals probably try to avoid such a provocative environment. Risk factors for motion sickness included younger age and higher MSSQ scores. Protective factors included prior Zero-G flight experience (habituation) and anti-motion sickness medication.

Platelets induce Pai-1 mRNA expression in monocytes through TGF-BETA

Introduction: Plasminogen activator inhibitor type-1 (PAI-1) is a physiological modulator of fibrinolysis. High plasma PAI-1 is associated with the 4G/5G promoter polymorphism and with increased cardiovascular risk. Here we explored the role of platelets in regulating expression of the PAI-1 gene in monocytes. Methods: Blood from PAI-1 4G/5G genotyped volunteers (n=6) was incubated with the platelet GPVI-specific agonist, cross-linked collagen related peptide (CRP-XL), in the presence or absence of Mab 9E1 that blocks the binding of P-selectin to PSGL1. Monocytes were isolated by +ve selection on CD14 beads and monocyte PAI-1 mRNA expression was measured by real-time PCR. Results: Activation of platelets with CRP-XL resulted in platelets binding to >70% of monocytes and was accompanied by >5000-fold induction of PAI-1 mRNA, peaking at 4hrs. PAI-1 expression was independent of the 4G/5G genotype. Blocking the binding of platelets to monocytes enhanced PAI-1 induction (p<0.05 at 4 hrs). Incubation of isolated monocytes with the releasate from CRP-XL stimulated platelets also led to PAI-1 mRNA expression. The platelet secretome contains >100 different proteins. To identify the soluble factor(s) responsible for induction of PAI-1, neutralizing antibodies to likely candidates were added to monocytes incubated with the platelet releasate. Anti- TGF-beta inhibited platelet releasate-mediated PAI-1 mRNA induction by >80%. Monocyte PAI-1 was also induced by stimulation of PSGL-1 with a P-selectin-Fc chimera, in the absence of platelets, which was also blocked by the TGF-beta antibody. Conclusions: These results suggest that platelets induce PAI-1 mRNA in monocytes predominantly via TGF-beta, released from both platelets, and monocytes via activation by PSGL-1 signalling.This stimulation is independent of 4G/5G genotype