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Approved for public release, distribution unlimited. / This thesis proposes a linear model based on human physiology for the explanation of the Motion Sickness Incidence (MSI) data found in previously reported experiments. The major human sensory systems taken into account are vestibular, visual, and the interaction between these two. The model is validated against the previous descriptive model and the corresponding experimental data. The proposed model predicts MSI with adequate precision (less than Å 5%) in the frequency range between 0.07 Hz and 0.25 Hz. The difference between the proposed model and the previous descriptive model is increased at the outer frequency regions of the data.

The Navy's use of high speed vessels such as HSV-2 SWIFT has raised questions of the effects of high speed motion on the ability of personnel to perform assigned duties. Performance degradation may occur during periods of excessive ship motion because of extreme motion sickness or periods of frequent task interruptions. With the use of high speed vessels expected to increase in the near future with the Littoral Combat Ship program, the issue of high speed motion effects on personnel becomes operationally relevant. This study will take a two part approach to analyze the effects of high speed motion: the motion sickness of SWIFT's crew and military passengers, and interruptions of task performance caused by vessel motion to critical watch stations. For the first part, statistical analysis will be used to determine relationships between ship motion and motion sickness. For the second part, modeling and simulation will be used to determine if there are watch stations that may be affected by varying levels of motion induced task interruptions. From this analysis, guidelines may be produced to describe the expected levels of motion sickness in personnel as well as watch stations in which personnel may have difficulties performing assigned duties.

Human Systems Integration Report / This study examined the effects of ship motion on motion sickness, adaptation, susceptibility, and performance. Data were collected onboard HSV-2 SWIFT during four periods from May 2004 to April 2005. HSV-2 SWIFT was chosen to examine performance on a high speed vessel with a catamaran hull type and a small crew. Data were collected using handheld personal digital assistants (PDAs) with a performance task along with questionnaires. There is a possibility that crewmember cognitive performance, as measured by Lapses on the Psychomotor Vigilance Task, may be related to reported Motion Sickness. Observations showed that adaptation to the ship motion occurred between day 2 and 3. Data collection periods found a relationship between the Motion History Questionnaire and motion sickness incidence. Lack of rough seas during the three of the data collection periods made it difficult to determine if there were more significant relationships during the analysis. Recommendations were to conduct future data collection during rough seas that have more variation in sea state and efforts should address how motion sickness affects crew performance and if crew performance is degraded to a level that will affect the shipâ s missions, specifically the LCSâ s missions of Surface Submarine Warfare, Mine Warfare, and high speed operations.

The presence of endotoxin in animals and humans triggers a sequence of acute phase responses, which include the synthesis and release of pro-inflammatory cytokines from immune cells, followed by the development of various symptoms of sickness including fever and an array of behavioural responses, commonly referred to as sickness behaviours. Most experimental investigations examining the mechanisms mediating fever and sickness behaviour responses have used purified lipopolysaccharide (LPS), the glycolipid pyrogenic moiety of the Gram-negative bacterial membrane, to trigger the innate immune system. Results obtained from studies using specific antagonists to block the action of cytokines synthesized following systemic administration of LPS, have uncovered important roles for pro-inflammatory cytokines, such as interleukin (IL)-1b, IL-6, tumour necrosis factor-alpha (TNF-a) and leptin, in mediating fever. Although it has been shown that administration of pro-inflammatory cytokines can induce sickness behaviour in experimental animals, no clear role has been identified for these cytokines as endogenous mediators of sickness behaviours induced following LPS administration. Using rats as experimental animals and endogenous cytokine antagonism, I therefore investigated whether endogenously released IL-1b, IL-6, TNF-a and leptin are physiologically active not only in the generation of fever, but also in the generation of two specific sickness behaviours, lethargy and anorexia, induced by subcutaneous (s.c.) administration of LPS. Lethargy, anorexia and fever were measured as changes in voluntary wheel-running, food intake and body temperature respectively. I antagonized the biological action of these cytokines in the periphery following s.c. administration of LPS by injecting rats intraperitoneally (i.p.) with specific anti-rat sera to one of the following: TNF-a, IL-1b, IL-6 or leptin. Peripherally-released leptin appeared to be an important mediator of both fever and anorexia, as the presence of leptin antibodies in the circulation abolished both the anorexia and fever induced by s.c. administration of LPS. In contrast though, whereas the presence of IL-6 antibodies in the circulation abolished the LPS-induced fever, suppression of voluntary activity was reversed by the presence of IL-6 antibodies only to the extent of 27%, and appetite also was not returned to normal levels in the presence of IL-6 antibodies. Thus, IL-6 may be an essential component of LPS-induced fever, but an additional factor or factors, possibly working in parallel with IL-6, may be required to mediate the lethargy and anorexia induced by s.c. administration of LPS. Injecting rats i.p. with TNF-a antiserum or IL-1b antiserum had no effect on LPS-induced lethargy and LPS-anorexia, indicating that if these cytokines are working with peripherally-released IL-6 to induce sickness behaviour, it is likely due to their synthesis in the brain. Injecting species-homologous rat IL-1β and IL-6 into the brains of conscious rats, I aimed to identify whether either of these two cytokines can act within the brain to induce lethargy and anorexia in the absence of an infection. Intracerebroventricular (i.c.v.) administration of either IL-1β or IL-6 before the night-time active period decreased voluntary activity in the rats in a dose-dependent fashion, whereas only IL-1β decreased food intake and body mass of the rats. It is possible therefore, that increased levels of IL-1β in the brain may be working in parallel with IL-6 released in the periphery to induce lethargy and anorexia following s.c. administration of LPS. Thus I antagonized the biological action of these cytokines endogenously by administering species-specific antiserum to IL-6 (IL-6AS) i.p., and a caspase-1 inhibitor, which prevents the cleavage of pro-IL-1β to biologically active IL-1β, i.c.v. and monitored the symptoms of sickness induced by LPS until they ceased, so as to determine the cytokine involvement not only in the induction of these responses, but also in the resolution of these responses. Pre-treating rats with either IL-6AS i.p. or a caspase-1 inhibitor i.c.v. attenuated the magnitude and the duration of the anorexia and lethargy induced by LPS administration. LPS-induced fever was completely abolished in rats pretreated i.p. with IL-6AS, while it was only partially attenuated in rats pre-treated i.c.v. with a caspase-1 inhibitor. In conclusion, there appears to be some distinct differences in the cytokine-mechanisms regulating fever and sickness behaviours induced by LPS. Identifying the physiological mechanisms mediating fever and sickness behaviours during illness may provide clinicians with more insight into managing not only the thermal, but also the non-thermal responses to infections, responses which may become detrimental to the host if they continue for a prolonged period. My observation that reducing either IL-6 in the circulation or IL-1β in the brain significantly enhances the resolution of anorexia and lethargy, but does not completely prevent them from occurring, appears to indicate that while individual cytokines are possible targets for therapies aimed at alleviating these sickness responses in patients with bacterial infections, to abolish them multiple cytokines may need to be targeted.

Thesis (M.Sc.(Agric.))(Genetics)--University of Pretoria, 2000. / Summary in English and Afrikaans Includes bibliographical references.

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