Die Multiple Sklerose (MS) ist eine chronisch-entzündliche Autoimmunerkrankung des zentralen Nervensystems (ZNS) und stellt die häufigste Ursache frühzeitiger Behinderung junger Erwachsener dar. Kennzeichnend sind multifokale ZNS-Läsionen, die durch Inflammation, Demyelinisierung und Axonschäden geprägt sind und zu multiplen neurologischen Defiziten führen. Derzeit ist es mithilfe der verlaufsmodifizierenden Therapie möglich, die Immunantwort abzuschwächen und damit die Krankheitsprogression zu verzögern. Geheilt werden kann die Erkrankung jedoch bislang nicht. Dabei ist nicht hinreichend geklärt, ob die neuen Therapieoptionen über die Immunmodulation/-suppression hinaus einen anhaltenden Schutz vor der langfristigen Neurodegeneration bieten. Basierend auf den vielversprechenden Ergebnissen klinischer Studien zur Therapie der schubförmig-remittierenden MS mit dem Anti-CD52-Antikörper Alemtuzumab, der zu einer Depletion CD52-exprimierender Immunzellen führt, wurden diesbezüglich Analysen in MS-Tiermodellen durchgeführt. Da die Untersuchung der zugrunde liegenden Patho- und Effektormechanismen am Menschen kaum möglich ist, ist die MS-Forschung für ein tiefergehendes Verständnis auf Tiermodelle angewiesen. Die experimentelle autoimmune Enzephalomyelitis (EAE) ist hierbei das am weitesten verbreitete Modell der MS, wofür vor allem der C57BL/6 (B6) -Mausstamm verwendet wird, da auf diesem Hintergrund die meisten genmodifizierten Mäuse gezüchtet werden. Jene tierexperimentellen Studien, in denen ein muriner Anti-CD52-Antikörper im frühen Krankheitsstadium der EAE (Auftreten erster paralytischer Symptome) verabreicht wurde, erbrachten den Hinweis einer neuroprotektiven und scheinbar regenerativen Wirkung des Antikörpers. Über einen neuroprotektiven Effekt von Alemtuzumab im schwer behandelbaren chronisch-progredienten Stadium der MS ist jedoch wenig bekannt. Die vorliegende Arbeit ist die erste detaillierte Untersuchung zum Einfluss des murinen Anti-CD52-Antikörpers auf die Demyelinisierung, den Axonschaden und die Hirnatrophie in der MP4-induzierten EAE der B6-Maus im chronischen Verlauf der Erkrankung (ab stabilem Plateau der klinischen Symptomatik). MP4 ist ein Myelinfusionsprotein aus MBP (Myelin-Basisches-Protein) und PLP (Proteolipidprotein), welches in B6-Mäusen durch aktive Immunisierung eine EAE induziert, die chronisch verläuft und als eines von wenigen Modellen neben der T-Zell-Abhängigkeit die an Bedeutung zunehmende B-Zell-Komponente der MS darstellt. Histopathologisch finden sich in der chronischen MP4-induzierten EAE eine ausgeprägte Rückenmarks- und Kleinhirnschädigung, die vor allem im Kleinhirn durch eine B-Zell-Aggregation charakterisiert ist. Nachdem die MP4-immunisierten Mäuse im chronischen Stadium der EAE an fünf aufeinanderfolgenden Tagen mit 10 mg/kg Körpergewicht murinem Anti-CD52-spezifischem IgG2a-Isotypantikörper bzw. murinem unspezifischem IgG2a-Isotyp-Kontroll-Antikörper behandelt worden waren, wurde die Lymphozytendepletion im peripheren Blut durchflusszytometrisch ermittelt und deren Einfluss auf MP4-spezifische Antikörper anhand eines indirekten Enzyme-linked Immunosorbent Assays (ELISAs) untersucht. Als Marker für Axonschäden wurde im Serum vorhandenes phosphoryliertes Neurofilament-Heavy (pNF-H) mithilfe eines indirekten Sandwich-ELISAs quantitativ bestimmt. Rückenmark und Kleinhirn wurden ultrastrukturell auf Veränderungen der Myelinisierung (mittels g-Ratio: Axondurchmesser geteilt durch Gesamtdurchmesser der Nervenfaser) und auf Axonpathologien (verringerter Abstand benachbarter Neurofilamente, axolytische Axone, axonaler Verlust) untersucht. Die Hirnatrophie wurde MRT-basiert gemessen und der klinische Verlauf täglich evaluiert. Durch die Anti-CD52-Antikörperbehandlung wurde die T- und B-Zellzahl zwar drastisch vermindert, die MP4-spezifische Antikörperproduktion blieb davon jedoch unbeeinträchtigt. Ein günstiger Effekt auf die De- und Remyelinisierung war nicht festzustellen. Das Hirnvolumen und die klinische Präsentation der Mäuse blieben ebenfalls unverändert. Während kein Unterschied der pNF-H-Konzentration zu erkennen war, konnte ultrastrukturell jedoch ein geringerer Axonschaden nachgewiesen werden. Insgesamt legen diese Ergebnisse nahe, dass der Anti-CD52-Antikörper im chronischen Verlauf der EAE/MS wenig Einfluss auf die neurodegenerativen Prozesse nimmt und die Regeneration nicht fördern kann. Die Ursache liegt vermutlich in der Undurchlässigkeit der Bluthirnschranke für Antikörper sowie dem limitierten Verständnis der Antikörperwirkung im ZNS. Die vorliegende Studie regt somit zur Etablierung von ZNS-wirksamen Antikörpern an und unterstreicht die Bedeutung der Entwicklung von selektiveren neuroprotektiven und remyelinisierungsfördernden Behandlungsansätzen, die eine wertvolle Ergänzung zur verlaufsmodifizierenden Therapie darstellen könnten. / Multiple sclerosis (MS) is a chronic inflammatory autoimmune disorder of the central nervous system (CNS) and the most frequent cause of early disabilities in young adults. Multifocal CNS lesions are typical for the disease and characterized by inflammation, demyelination and axonal pathology that lead to multiple neurological deficits. Currently disease modifying therapies (DMTs) make it possible to reduce the immune response and to delay the progression of the disease, but there is still no cure for MS. However, it is not fully understood whether these new treatment options provide long-lasting protection against neurodegeneration beyond immune modulation/-suppression. Based on promising data from clinical studies of the anti-CD52 antibody alemtuzumab for the treatment of relapsing-remitting MS that leads to depletion of CD52-expressing lymphocytes, investigations on this question were performed in animal models for MS. Since studies of the underlying pathomechanisms and effector functions are difficult to carry out in humans, MS research is still dependent on animal models to gain deeper understanding. Experimental autoimmune encephalomyelitis (EAE) is the most widely distributed model for MS, for which the C57BL/6 (B6) mouse strain is commonly used, since most gene-modified mice are bred on this background. The animal experiments that applied a murine anti-CD52 antibody at early disease stage of EAE (first appearance of paralytic symptoms) indicated a neuroprotective and apparent regenerative effect of the antibody. Indeed, little is known about a neuroprotective effect of alemtuzumab when given at the chronic progressive phase of MS which is still difficult to treat. The present study is the first detailed investigation on the impact of the murine anti-CD52 antibody on demyelination, axonal damage and brain atrophy in MP4-induced EAE in B6 mice during the chronic stage of the disease (starting at stable plateau of clinical symptoms). MP4 is a myelin fusion protein of MBP (myelin basic protein) and PLP (proteolipid protein) that induces chronic EAE in B6 mice via active immunization. MP4-induced EAE is one of the few models that reflects the B cell component in addition to the T cell-mediated features of MS. Its chronic stage is characterized by severe spinal cord and cerebellar pathology with B cell aggregation especially in the cerebellum. After MP4-induced mice were treated at the chronic stage of EAE either with 10 mg/kg body weight murine anti-CD52 specific IgG2a isotype antibody or murine unspecific IgG2a isotype control antibody for five consecutive days, flow cytometric analysis of lymphocyte depletion was performed on peripheral blood and its effect on MP4-specific antibodies was determined by indirect enzyme-linked immunosorbent assay (ELISA). The level of released phosphorylated neurofilament-heavy (pNF-H) in the serum as a marker for axonal damage was measured by indirect Sandwich-ELISA. Change of myelination (by using the g-ratio: axon diameter divided by nerve fiber diameter) and axonal pathology (decreased nearest neighbour neurofilament distance, axolytic axons, axonal loss) was evaluated in spinal cord and cerebellum by electron microscopy. Brain atrophy was measured based on MRI and clinical course was daily evaluated. The treatment with the anti-CD52 antibody drastically reduced the number of T cells and B cells, while the titers of MP4-specific antibodies remained unaffected. There was no effect on de- and remyelination. Furthermore, brain volume and clinical disease severity remained unaltered. While there was no difference in pNF-H concentration, on the ultrastructural level the number of damaged axons was decreased. In sum, these data reveal that the anti-CD52 antibody has a low impact on neurodegenerative processes and none on regeneration in the chronic stage of EAE/MS. This is probably due to the impermeability of the blood-brain barrier for antibodies and the limited understanding of the effects of antibody treatment in the CNS. Thus, this study points towards the need for effective antibody treatment in the CNS as well as for more selective neuroprotective and remyelination promoting therapeutic strategies that could complement the existing DMTs.

Die Multiple Sklerose ist eine bisher nicht heilbare, chronisch-inflammatorische demyelinisierende Erkrankung des zentralen Nervensystems. Trotz intensiver Forschungsbemühungen ist der exakte Pathomechanismus nicht vollkommen verstanden. Klar ist jedoch, dass der Blut-Hirn-Schranke eine entscheidende Rolle bei der Pathogenese zukommt. Seit Februar 2014 ist mit Dimethylfumarat ein neues orales Medikament für die schubförmige Multiple Sklerose zugelassen. Die Wirkungen von Fumarsäureestern auf humane zerebrale Endothelzellen als Grundsteine der Blut-Hirn-Schranke sind allerdings nur unzureichend untersucht. Mehrere Forschungsgruppen demonstrierten an humanem Nabelschnurvenenendothel einen hemmenden Effekt von Fumarsäureestern auf die Adhäsion von Leukozyten und beschrieben eine Inhibition der Aktivierung des proinflammatorischen Transkriptionsfaktors NFB in den Endothelzellen. Aufgrund der charakteristischen Eigenschaften zerebralen Endothels ist eine Übertragung dieser Beobachtungen auf die Blut-Hirn-Schranke allerdings nicht ohne weiteres möglich. Daher galt es potentielle Effekte von Fumarsäureestern auf primäre humane zerebrale Endothelzellen als in vitro Modell der Blut-Hirn-Schranke zu überprüfen. Dabei wurden die Zellen nicht nur unter ruhenden Bedingungen, sondern auch unter inflammatorischer Stimulation mit TNF-α, IL-1 und IFN untersucht, einem Milieu, wie es in inflammatorischen MS Läsionen zu finden ist. In Leukozyten-Adhäsionsassays konnte durch Inkubation mit Monomethylfumarat und Dimethylfumarat keine funktionale Beeinflussung der Adhäsion von T-Lymphozyten an den verwendeten zerebralen Endothelzellen verzeichnet werden. Kongruent dazu fand sich in durchflusszytometrischen Analysen keine Hemmung der inflammatorisch vermittelten Expression des Adhäsionsmoleküls ICAM-1, welches eine tragende Rolle bei der Leukozytenmigration spielt. Inflammatorische intrazelluläre Signalwege, wie die NFB-Kerntranslokation oder die Phosphorylierung von p38 wurden in HECE im Gegensatz zu HUVEC durch Fumarsäureester ebenso wenig beeinflusst. Diese in sich konsistenten Ergebnisse führen zu der Schlussfolgerung, dass im Gegensatz zu anderen Gefäßbetten weder Dimethylfumarat noch Monomethylfumarat direkt am zerebralen Endothel anti-inflammatorisch wirken. / Dimethyl fumarate (DMF) is approved for disease-modifying treatment of patients with relapsing-remitting multiple sclerosis. Animal experiments suggested that part of its therapeutic effect is due to a reduction of T-cell infiltration of the central nervous system (CNS) by uncertain mechanisms. Here we evaluated whether DMF and its primary metabolite monomethyl fumarate (MMF) modulate pro-inflammatory intracellular signaling and T-cell adhesiveness of nonimmortalized single donor human brain microvascular endothelial cells at low passages. Neither DMF nor MMF at concentrations of 10 or 50 μM blocked the IL-1β-induced nuclear translocation of NF-κB/p65, whereas the higher concentration of DMF inhibited the nuclear entry of p65 in human umbilical vein endothelium cultured in parallel. DMF and MMF also did not alter the IL-1β-stimulated activation of p38 MAPK in brain endothelium. Furthermore, neither DMF nor MMF reduced the basal or IL-1β-inducible expression of ICAM-1. In accordance, both fumaric acid esters did not reduce the adhesion of activated Jurkat T cells to brain endothelium under basal or inflammatory conditions. Therefore, brain endothelial cells probably do not directly mediate a potential blocking effect of fumaric acid esters on the inflammatory infiltration of the CNS by T cells.

Bei Patienten, die an einer speziellen Form der MS erkrankten, konnten Entzündungsinfiltrate in den Meningen nachgewiesen werden, die in ihrem Aufbau lymphoidem Gewebe ähnelten. Das Auftreten dieser Infiltrate war mit einem schwereren Krankheitsverlauf assoziiert. Das Mausmodell der B-Zell-abhängigen MP4-induzierten experimentellen autoimmunen Enzephalomyelitis (EAE) zeigt in den Kleinhirnen der Mäuse Infiltrate, die den Infiltraten beim Menschen ähneln. Wir nutzten die MP4-induzierte EAE, um die Mechanismen der Erkrankungsentstehung und Progression besser zu verstehen. Ziel dieser Arbeit war es intakte und stabile Ribonukleinsäuren (RNA) aus den Infiltraten der Mäuse zu isolieren. Sowie Identifizierung von Gene, die während verschiedener Stadien der zerebralen Entzündungsreaktion hochreguliert waren. Wir verglichen die Möglichkeiten der RNA-Isolation bei Paraffin-eingebettetem Gewebe und kryofixiertem Gewebe. Um die Vergleichbarkeit der Qualitäts- und Quantitätsanalyse zu gewährleisten, wurde für jede Probe eine RNA Integritätsnummer (RIN) ermittelt. Wir führten eine Laser Capture Microdissection (LCM) und anschließende Gensequenzierung der zerebralen Infiltrate bei Mäusen durch, bei denen eine MP4-abhängige EAE ausgelöst wurde. Des Weiteren verglichen wir die Ergebnisse mit den Expressionsprofilen von sekundär lymphatischen Organen (SLOs). Insgesamt konnten wir 43 Gene herausfiltern, die im Vergleich zu den Kontrollgruppen hochreguliert waren. Die Entwicklung von ektopen lymphatischen Strukturen (ELS) im zentralen Nervensystem (ZNS) ist ein komplexer und bisher wenig verstandener Prozess. In dieser Studie beobachteten wir 43 Gene, die während der Entwicklung von B- Zell-Infiltraten in den Kleinhirnen von MP4-immunisierten Mäusen signifikant hochreguliert waren. Von diesen Genen wurden bereits 14 im Zusammenhang mit der MS erwähnt und sind zum Teil Gegenstand aktiver Forschung. / In patients suffering from a specific form of MS, inflammatory infiltrates were detected in the meninges, which were similar in their structure to lymphoid tissue. The presence of these infiltrates was associated with a more severe disease progression. The mouse model of B-cell-dependent MP4-induced experimental autoimmune encephalomyelitis (EAE) shows infiltrates in the cerebellums of mice that are similar in structure and organization to infiltrates in humans. The aim of this work was first to isolate intact and stable ribonucleic acids (RNA) from mouse infiltrates. We then identified genes that were upregulated in the B-cell infiltrates during the cerebral inflammatory response. We compared the potential for RNA isolation in paraffin-embedded tissue and cryofixed tissue. We performed laser capture microdissection (LCM) followed by gene sequencing of cerebral B-cell infiltrates in mice. MOG:35-55-induced EAE was used as a B-cell-independent control model. Furthermore, we compared the results with the expression profiles of secondary lymphoid organs. RNA isolation from cryofixed tissue was superior to that from paraffin-embedded tissue. In this study, we observed 43 genes that were significantly upregulated during the development of B-cell infiltrates in the cerebellums of MP4-immunized mice. Of these genes, 14 have already been mentioned in the context of MS and some are the subject of active research. However, some of the remaining genes also show promising immunological properties. The exact role of the genes and possibly their influence on each other offer great scope for further research.

Multiple sclerosis (MS) is an immune-mediated disorder characterized by neuroinflammation, demyelination, and neurodegeneration that results in the degradation of neurological structures within the central nervous system (CNS). This degradation of neurological structures often has a substantial impact on the ambulatory abilities of people living with MS, with an estimated 30% of the MS population requiring a wheelchair for mobility (i.e., nonambulatory). Unfortunately, current pharmacological interventions have limited efficacy for those with progressed disability and alternative strategies for disease management must be considered, such as exercise training. To date, most of the MS exercise training literature has not focused on nonambulatory people with MS, limiting evidence-based exercise recommendations for this population. As such, the central purpose of this dissertation was to inform exercise prescription and delivery for nonambulatory people with MS. In order to achieve this goal, three studies were conducted. The first study in this dissertation (presented across two manuscripts) evaluated the safety and physiological response of nonambulatory people with MS to three adapted exercise modalities (arm cycle ergometer, recumbent stepper, functional electrical stimulation cycle). This study determined that acute adapted exercise was well-tolerated by nonambulatory people with MS, with few adverse events reported across all exercise sessions. Notably, participants favoured recumbent stepper and functional electrical stimulation cycling exercise over arm cycle ergometer exercise. Further, participants were capable of exercising at an intensity that satisfied the American College of Sport Medicine’s criteria for moderate-to-vigorous physical activity on all adapted modalities. This suggests all tested modalities are capable of promoting improvements in health-related fitness outcomes. The second study, a systematic review and meta-analysis, explored outcome measures that capture ‘participation’ in MS exercise trials, and the influence of exercise training on ‘participation’. Described within the International Classification of Functioning, Disability and Health (ICF) as the “involvement in life situations”, ‘participation’ outcomes provide insight into the impact of MS on everyday life. Findings from this study demonstrated variability in how ‘participation’ has been captured, with an emphasis on items describing ‘mobility’. Further, the meta-analysis revealed that exercise training had a moderate, positive effect on outcomes that capture participation, a novel finding regarding the benefits of exercise training in MS. The final study of this dissertation, an online-based survey, identified perceived exercise benefits, barriers, and needs among nonambulatory people with MS. This study demonstrated that nonambulatory people with MS perceive health improvements and personal accomplishments as the greatest benefits associated with exercise engagement. The sample also cited environmental challenges and MS symptoms as prominent barriers to exercise engagement. The current sample identified that exercise facilities, specifically exercise equipment, were failing to accommodate their exercise needs. Collectively, the findings from this dissertation will help address prominent gaps in the exercise training literature involving nonambulatory people with MS. Addressing such gaps will contribute to advancing evidence-informed exercise interventions, promoting measurable health improvements, and ultimately increasing engagement in exercise for nonambulatory people with MS,

No description available.

This thesis proposes a novel multiple traffic light recognition system based on videos captured by a monocular camera. Advanced driver assistance system (ADAS) and autonomous driving system (ADS) are becoming increasingly important to help drivers maneuvering vehicles and increase the vehicle and road safety in modern life. Traffic light recognition system is a significant part of ADAS and ADS, which can detect traffic light on the road and recognize different types of traffic lights to provide useful signal information for drivers. The proposed method can be applied to real complex environment only based on a monocular camera and is tested in real-world scenarios. This system consists of three parts: multiple traffic light detection, multi-target tracking and state classification. For the first step, a supervised machine learning method, support vector machine (SVM) with two integral features - histogram of oriented gradients (HOG) and histogram of CIELAB color space (HCIELAB), are used to detect traffic lights in the captured image. Then, a new multi-target tracking algorithm is presented to improve the accuracy of detection, reduce the number of false alarm and missing targets, by means of nearest neighbor data association, motion model analysis and Lucas-Kanade optical flow tracking and the region of interest (ROI) prediction. Finally, a SVM-based and a convolution neural network (CNN) based classifiers are introduced to classify the state of traffic lights, that provides the stop, go, warning, straight and turn information. Various experiments have been conducted to demonstrate the practicability of the proposed method. Both GPU-based and CPU-based programming can run real-time on the real street environment. / Thesis / Master of Applied Science (MASc)

Multiple Sclerosis (MS) is an autoimmune disease characterized by demyelination and axon degeneration of the central nervous system that is accompanied by a wide range of symptoms. It is well established that physical activity is associated with a wide variety of health benefits, including improving fitness, MS-related symptoms and function in the MS population. However, despite the potential benefits associated with physical activity participation, most people living with MS remain physically inactive. In 2012, new evidence-based physical activity guidelines (PAGs) for adults with MS were released. The PAGs suggest that for health benefits, adults aged 18-64 years with mild to moderate disability need at least 30 minutes of moderate intensity aerobic physical activity two days per week and strength training for major muscle groups two times per week. The purpose of this dissertation was to determine the association between physical activity and health and to explore physical activity as a potential disease-modifying therapy in the MS population. This was completed through a series of three projects focusing on the PAGs for adults with MS. The focus of the first study of this dissertation was on the implementation of the PAGs. The results from this study revealed that direct referral to physical activity from a physician is twice as effective as simply providing information about physical activity with respect to adhering to the PAG recommendations in people with MS (65.2 % vs. 32.8 % for direct referral and control groups, respectively). Further, the results revealed that a high self-efficacy for exercise at baseline may be an additional predictor to PAG adherence. The purpose of the second study of this dissertation was to validate the PAGs for people with MS within a community-based intervention, and to affirm that following the PAGs for 16 weeks would result in improvements in fitness, mobility, fatigue symptoms and quality of life. The results from the second study confirm the effectiveness of the PAGs for people with MS for improving health, as significant improvements were observed in VO2 peak (+32 %), strength (+8-20 %), mobility (+14 %), fatigue symptoms (-40 %) and quality of life (+10-24 %). The purpose of the third and final study was to determine the effect of exercise on brain function and cognition in a sample of adults living with MS. Following the PAGs for 16 weeks led to significant improvements in processing speed and memory in adults living with MS. Overall, the results from this dissertation are extremely promising and highlight the importance of physical activity with respect to improving aspects of health and the effect it can have on MS-related symptoms and cognition in the MS population. Novel findings in this dissertation present convincing evidence that physicians should refer patients with MS to participate in exercise to improve MS-related symptoms and overall well-being. / Thesis / Doctor of Philosophy (PhD)

Le myélome multiple est un cancer incurable caractérisé par une accumulation de plasmocytes malins dans la moelle osseuse. Récemment, nous avons découvert que l'expression forcée du facteur de transcription PAX5 (paired box protein 5) dans des lignées cellulaires humaines de myélome multiple induisait une forte diminution de la viabilité cellulaire. Des viabilités de près de 50% ont été observées dans les lignées cellulaires de myélome multiple RPMI-8226 et U266 aux jours quatre et sept respectivement après l'infection de ces cellules par un vecteur adenoviral codant pour PAX5. Nous avons constaté que la mortalité était due à l'apoptose induite par une baisse de MCL-1 (myeloid cell leukemia-1). La spécificité de cet effet a été démontrée grâce à des lignées cellulaires de leucémie à plasmocytes, lignées cellulaires dont la viabilité ne variait pas suite à l'expression forcée de PAX5, suggérant ainsi une nouvelle avenue de traitement du myélome multiple.

The study explored the nature of the involvement of certain demographic (gender, age and education), cognitive (specifically executive functions) and psychological factors (personality changes and other psychosocial issues) in the disease process in a group of MS patients. A sample of 20 adults (8 male and 12 female) with a mean age of 47,65 years was employed. The assessments procedure entailed a set of neuropsychological measures, a 16 PF questionnaire and a semi-structured interview (with a significant other) from which certain qualitative themes were extracted. The MS sufferers showed deficiencies on measures of executive function, a 16 PF profile in accordance with that of individuals with physical illness and the qualitative themes revolved around issues such as mood, independence, work-status, self-confidence and cognitive difficulties. The data resulting from these assessments supported one another and served to enrich our knowledge regarding the life world of the person with MS. / Psychology / MSc. (Psychology)

ITC/USA 2010 Conference Proceedings / The Forty-Sixth Annual International Telemetering Conference and Technical Exhibition / October 25-28, 2010 / Town and Country Resort & Convention Center, San Diego, California / This paper investigates the performance of a multiple-input multiple-output (MIMO) digital communication system, when the transmitter is located on a spinning vehicle. In particular, a 2x2 MIMO system is used, with Alamouti coding at the transmitter. Both Rayleigh and Rayleigh plus line-of-sight, or Rician, models combined with a deterministic model to simulate the channel. The spinning of the transmitting vehicle, relative to the stationary receive antennas, modulates the signal, and complicates the decoding and channel parameter estimation processes. The simulated system bit error rate is the primary performance metric used. The Alamouti channel code is shown to perform better than the maximal ratio receiver combining (MRRC) and single receiver (2x1) system in some circumstances and performs similarly to the MRRC in the broadside case.