Dementia is a clinical state caused by neurodegeneration and characterized by a loss of function in cognitive domains and behavior. Alzheimer’s disease (AD) is the most common form of dementia. Although the amyloid β (Aβ) protein and hyperphosphorylated tau aggregates in the brain are considered to be the key pathological hallmarks of AD, the exact cause of AD is yet to be identified. In addition, clinical diagnoses of AD can be error prone. Many previous studies have compared the clinical diagnosis of AD against the gold standard of autopsy confirmation and shown substantial AD misdiagnosis Hippocampal sclerosis of aging (HS-Aging) is one type of dementia that is often clinically misdiagnosed as AD. AD and HS-Aging are controlled by different genetic architectures. Familial AD, which often occurs early in life, is linked to mainly mutations in three genes: APP, PSEN1, and PSEN2. Late-onset AD (LOAD) is strongly associated with the ε4 allele of apolipoprotein E (APOE) gene. In addition to the APOE gene, genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) in or close to some genes associated with LOAD. On the other hand, GRN, TMEM106B, ABCC9, and KCNMB2 have been reported to harbor risk alleles associated with HS-Aging pathology. Although GWAS have succeeded in revealing numerous susceptibility variants for dementias, it is an ongoing challenge to identify functional loci and to understand how they contribute to dementia pathogenesis. Until recently, rare variants were not investigated comprehensively. GWAS rely on genotype imputation which is not reliable for rare variants. Therefore, imputed rare variants are typically removed from GWAS analysis. Recent advances in sequencing technologies enable accurate genotyping of rare variants, thus potentially improving our understanding the role of rare variants on disease. There are significant computational and statistical challenges for these sequencing studies. Traditional single variant-based association tests are underpowered to detect rare variant associations. Instead, more powerful and computationally efficient approaches for aggregating the effects of rare variants have become a standard approach for association testing. The sequence-kernel association test (SKAT) is one of the most powerful rare variant analysis methods. A recently-proposed scan-statistic-based test is another approach to detect the location of rare variant clusters influencing disease. In the first study, we examined the gene-based associations of the four putative risk genes, GRN, TMEM106B, ABCC9, and KCNMB2 with HS-aging pathology. We analyzed haplotype associations of a targeted ABCC9 region with HS-Aging pathology and with ABCC9 gene expression. In the second study, we elucidated the role of the non-coding SNPs identified in the International Genomics of Alzheimer’s Project (IGAP) consortium GWAS within a systems genetics framework to understand the flow of biological information underlying AD. In the last study, we identified genetic regions which contain rare variants associated with AD using a scan-statistic-based approach.

GB virus C (GBV-C) is a nonpathogenic lymphotropic virus that replicates in B and T lymphocytes. Infection with GBV-C is documented worldwide and is common: between 1% and 5% of healthy blood donors are viremic at the time of donation. Antibodies to GBV-C proteins are not usually detected during viremia, and antibodies to the GBV-C envelope glycoprotein E2 develop following the clearance of viremia. Although GBV-C viremia may persist for decades, viremia usually clears within 2 years following infection in the majority of individuals infected by blood transfusion. A chimpanzee variant of GBV-C, designated GBV-Ccpz, is found in captive and noncaptive chimpanzees and its prevalence and natural history are uncharacterized. GBV-C research was initially performed by viral hepatitis research groups because it was predicted to cause hepatitis. The realization that GBV-C did not cause hepatitis resulted in a marked reduction in research activity. Because Hepatitis C virus co-infection worsens the clinical course of HIV-infected patients, researchers hypothesized that the related virus, GBV-C, may impact HIV disease. In 1998, researchers found that HIV-infected individuals who were co-infected with GBV-C survived longer than those without GBV-C. These findings provide the rationale for examining the relationship of GBV-C and HIV and the development of GBV-C as a novel therapeutic for HIV. GBV-C infection of PBMCs inhibits the replication of HIV isolates and one of the mechanisms for this is the induction of the release of soluble ligands for HIV entry receptors (RANTES, macrophage inflammatory proteins (MIP)-1α and MIP-1β and SDF-1) by GBV-C. The GBV-C envelope glycoprotein E2 contributes directly to the inhibition of HIV infection. Incubation of recombinant E2 with PBMCs at 4°C prior to HIV infection results in a decrease in HIV replication, and only HIV gp160 enveloped pseudoparticle transduction, not VSV-G enveloped pseudoparticle transduction, is inhibited by GBV-C E2. This suggests that GBV-C E2 inhibits HIV infection at an entry step when the HIV gp160 envelope protein interacts with cellular receptors and membranes. How GBV-C E2 interacts with cellular surfaces and which cellular proteins are utilized for GBV-C binding and entry are unknown. Here, we characterize GBV-C E2 binding to human PBMCs, murine cells, and multiple transformed cell lines to identify the PBMC subset which E2 binds and to identify candidate cellular receptors involved in GBV-C binding and entry. Understanding how GBV-C E2 interacts with cellular surfaces is critical to determining how it inhibits HIV entry. Anti-GBV-C E2 antibodies are also associated with improved survival in HIV-infected individuals. Recent studies demonstrated that anti-E2 antibodies neutralize HIV infection in vitro and immunoprecipitate HIV virions. In these studies, we describe how anti-E2 antibodies immunoprecipitate retroviral particles regardless of the specific viral envelope protein on the surface, but only neutralize particles bearing the HIV gp160 envelope protein. We also found that the cellular antigen recognized by anti-E2 antibodies is accessible only in permeabilized cells and not on the cell surface. These studies provide insight into the HIV-inhibitory mechanisms of anti-E2 antibodies, which should aid in the development of GBV-C E2 as an immunogen in an HIV vaccine. Finally, no animal models exist for studying GBV-C infection or GBV-C vaccines as HIV therapeutics in vivo. We examined the natural history GBV-Ccpz in a captive chimpanzee population, and found that the prevalence of GBV-Ccpz viremia and anti-E2 antibodies, as well as the length of persistent infection, were similar to those found in healthy human blood donors. The GBV-Ccpz 5#8217;ntr and RdRp sequences from chimpanzee subspecies troglodytes and verus shared a high level of sequence identity and indicate that the chimpanzee variant should be designated GBV-Ccpz rather than the currently used GBV-Ctrog. These findings demonstrate that GBV-Ccpz viremia and E2 antibody status should be tested in animals involved in clinical research trials because affected animals may have altered responses to GBV-C infection or HIV vaccines, and that the chimpanzee would be a good animal model in which to study GBV-C infection.

L'organisation de l'ADN sous forme de nucléosome interfère avec différents processus cellulaires. La cellule recrute des facteurs de remodelage et des variants d'histones pour surmonter cette barrière physique. Dans ce travail, nous utilisons la Microscopie à Force Atomique pour visualiser des mono- et des oligo- nucléosomes à l'équilibre et hors-équilibre.<br />Nous montrons que le variant H2A.Bbd modifie la structure et la dynamique du mono-nucléosome et que sa présence altère la faculté de la chromatine à former une structure d'ordre supérieur. En utilisant un modèle physique nous expliquons quantitativement ce comportement par la flexibilité du mono-nucléosome.<br />Nous étudions ensuite le mécanisme du remodelage de mono-nucléosomes par SWI/SNF et RSC. Nous mettons en évidence un intermédiaire réactionnel sous la forme d'un nucléosome sur-complexé apparaissant avant le nucléosome glissé. Enfin au niveau des di-nucléosomes nous montrons que RSC est un ‘randomiseur' processif et séquentiel.

Chaque spermatozoïde transmet non seulement le génome paternel, mais également une information épigénétique, portée par l'organisation structurale du génome, ou épigénome. Malgré son importance lors du développement embryonnaire, peu de données décrivent l'épigénome transmis par le gamète mâle. Ce travail étudie la reprogrammation de l'épigénome lors de la différenciation post-méiotique des cellules germinales males, ou spermiogenèse. Ce processus implique une restructuration globale de la chromatine caractérisée par l'enlèvement de la majorité des histones, associées à l'ADN dans les cellules somatiques, et leur remplacement par des protéines nucléaires spécifiques du gamète male. <br />Ce travail met en évidence dans les cellules post-méiotiques, un dialogue original entre les modifications post-traductionnelles des histones et la présence de nouveaux variants d'histones associés à l'hétérochromatine péricentrique. La reprogrammation épigénétique des régions de contrôle de l'empreinte parentale a également été analysée. De plus, de nouvelles fonctions ont été mises en évidence pour plusieurs protéines chaperones, notamment HSP70.2, Npm3 et NAP1L4, qui seraient impliquées dans l'incorporation de variants d'histones ou de protéines basiques spécifiques lors des étapes tardives de la spermiogenèse.<br />Ainsi, l'action coordonnée de plusieurs voies de réorganisation de la chromatine participe à la mise en place de l'épigénome transmis par les spermatozoïdes.

Zur Zeit leiden ca. 24 Millionen Menschen auf der ganzen Welt unter Demenz, Alzheimer macht dabei 50-60% aller Demenzfälle aus. Da der Anteil der Bevölkerung, der an Demenz leidet, proportional zum Alter zunimmt und der Anteil älterer Menschen in der Gesellschaft von Jahr zu Jahr steigt, wird Alzheimer immer mehr zu einem ernstzunehmenden, gesellschaftlichen Problem. Zum Stand der heutigen Forschung ist es etabliert, dass die Aminosäure Glutamat - quantitativ einer der wichtigsten Neurotransmitter im Zentralen Nervensystem (ZNS) - toxische Konzentrationen erreichen kann wenn sie - im Zuge der Übertragung von Aktionspotentialen - nach ihrer Freisetzung nicht aus dem Synaptischen Spalt entfernt wird. Viele Studien haben gezeigt, dass in der Alzheimerschen Krankheit die Glutamataufnahme beeinträchtigt ist, was zu toxischen Konzentrationen von Glutamat und dem daraus folgenden Absterben von Neuronen führt. Der exitatorische Aminosäuretransporter 1 (EAAT1) gehört zu der Familie der Na+-abhängigen Glutamattransporter und stellt nach EAAT2 den quantitativ wichtigsten Glutamattransporter im ZNS dar. In diesem Projekt wurde eine bis dahin für den Menschen nicht bekannte EAAT1 Spleißvariante, in der Exon 3 ausgeschnitten wird, nachgewiesen. Diese Variante wurde EAAT1Δ3 genannt und stellt damit mit EAAT1Δ9 die zweite für EAAT1 nachgewiesene Spleißvariante dar. Eine auf real-time RT-PCR basierende Methode wurde entwickelt, um die Transkripte von EAAT1 wildtyp (EAAT1 wt), EAAT1Δ3 und EAAT1Δ9 zu quantifizieren. Proben aus verschiedenen Hirnarealen wurden aus einem Set von Kontrollen und Alzheimerfällen bei der Quantifizierung verwendet. Die gewählten Areale sind von der Alzheimerschen Krankheit unterschiedlich stark betroffen. Dies diente als interne Kontrolle für die durchgeführten Experimente und ermöglichte so die Differenzierung zwischen beobachteten Effekten: Nur Effekte die alleinig in von Alzheimer betroffenen Gehirnarealen auftreten, können als spezifisch für die Krankheit angesehen werden. Die Resultate diese Projektes zeigen, dass EAAT1Δ3 in sehr geringer Anzahl transkribiert wird, die nur 0.15% der EAAT1 wt Transkription entspricht. Dahingegen entspricht das EAAT1 Δ9 Transkript im Durchschnitt 26.6% des EAAT1 wt Transkripts. Es wurde nachgewiesen, dass die Transkriptionsrate aller EAAT1 Varianten in Alzheimerfällen signifikant reduziert ist (P<0.0001). Dies unterstützt die Theorie, dass bei Alzheimerfällen die EAAT1 Proteinexpression stark reduziert und der Glutamattransport, der normalerweise durch diesen Transporter gewährleistet wird, stark eingeschränkt ist. Dies wiederum resultiert in toxisch hohen Glutamatkonzentrationen und damit dem Absterben von Neuronen. Die gefundene Reduktion der EAAT1Transkription ist nicht spezifisch für Gehirnareale die von Alzheimer betroffen sind, sondern tritt in selbem Maße in nicht von Alzheimer betroffenen Gehirnarealen auf. Daraus lässt sich schließen, dass die Reduktion der EAAT1 Transkription eher ein Resultat eines in der Alzheimerschen Krankheit präsenten, grundlegenden Krankheitsmechanismus ist als deren Ursache. / Today about 24 Million people worldwide suffer from dementia, Alzheimer’s Disease accounts for approximately 50-60% of all dementia cases. As the prevalence of dementia grows with increasing age Alzheimer’s Disease becomes more and more of an issue for society as the proportion of elderly people increases from year to year. It is well established, that the amino acid glutamate - quantitatively being the most important neurotransmitter in the central nervous system (CNS) - may reach toxic concentrations if not cleared from the synaptic cleft into which it is released during transmittance of action potentials. In Alzheimer’s Disease there is strong evidence for a generally impaired glutamate uptake system which in turn is thought to result in toxic levels of the amino acid with the potential to kill off neurons. The excitatory amino acid transporter 1 (EAAT1) belongs to the family of Na+-dependent glutamate transporter and accounts together with EAAT2 for most of the glutamate uptake in the CNS. In this project a new splice variant of EAAT1, skipping exon 3 was detected in human brain samples and subsequently called EAAT1Δ3, this being the second splice variant found after the recent detection of EAAT1Δ9. A method was developed to quantify the transcript of EAAT1 wt, EAAT1Δ3 and EAAT1Δ9 by means of real-time PCR. Samples were taken from different brain areas of a set of control and AD cases. The areas chosen for examination are affected differently in Alzheimer’s Disease, this was used an internal control for the experiments done in this project as to determine whether any effect observed is specific for AD, i.e. AD affected areas or is generally seen in all areas examined. The results of this project show that EAAT1Δ3 is transcribed in very low copy numbers making up a proportion of 0.15% of EAAT1 wt whereas EAAT1Δ9 is transcribed in a considerably large proportion of EAAT1 wt of 26.6%. It was moreover found that all EAAT1 variants are transcribed at significantly lower rates (P<0.0001) in AD cases, supporting the theory that EAAT1 protein expression is reduced to a point where glutamate uptake normally mediated by this transporter is impaired. This in turn is thought to result in toxic levels glutamate accounting for neuronal loss in the disease. No area-dependent effects were found, suggesting that the reduction of EAAT1 transcription is rather a result of an underlying general mechanism present in AD. Further research will have to be done to assess the degree of EAAT1 expression in AD and whether those future findings match with the result of this project.

Le cancer colorectal (CCR) est le troisième cancer dans le monde et devenu un véritable enjeu de santé publique. Environ 5% sont associés à une forme familiale : la polypose adénomateuse familiale, le Syndrome de Lynch et la MAP (MUTYH-Associated Polyposis). Implication du syndrome MAP dans les polyposes: Parmi 31 patients avec une polypose sans mutation sur APC, 6 (20%) présentaient une mutation biallélique sur MUTYH. Fréquence de la mutation c.1185_1186dup dans les MAP: Au sein d'un groupe de 36 familles mutées sur MUTYH, 11 avaient une mutation biallélique homozygote c.1185_1186dup. Cette mutation était significativement plus fréquemment observée chez les patients d'Afrique du Nord (79% vs. 5%, p<0,0001). La recherche d'un haplotype commun en utilisant 10 microsatellites a identifié un segment de 1,3 cM présent chez tous les patients avec la mutation c.1185_1186dup. Variants rares (VR) de la cycline D1 : La comparaison des fréquences alléliques des VR de la cycline D1 fut réalisée entre les cas (112 patients avec une polypose indéterminée et 44 avec un CCR précoce) et 866 témoins. Les VR étaient plus fréquemment observés dans le groupe de malades. En combinant les VR, une augmentation du risque était retrouvée pour le groupe de patients avec une polypose indéterminée: (OR=2,2); 95%IC, 1,1-4,4; P=0,03). Rôle des variants rares : 70 variants provenant de 17 gènes ont été examinés au sein de la même population. 21 était des VR (fréquence<1%) et 4 étaient plus fréquemment observés chez les cas (EXO1-12, MLH1-1, CTNNB1-1 et BRCA2-37, p<0,05). En combinant tous les VR avec une fréquence allélique <0,5%, un sur risque de 3,2 était observé (95%CI=1,1-9,5; p=0,04)

L'organisation en chromatine permet de compacter l'ADN génomique et de réguler finement l'expression du génome. La particule cœur du nucléosome, composée d'un octamère de protéines histones autour desquelles s'enroule l'ADN, peut être modulée par l'incorporation de variants d'histones. Pour l'histone H3, les variants réplicatifs H3.1 et H3.2 permettent une incorporation lors de la réplication de l'ADN, tandis que le variant H3.3 est incorporé tout au long du cycle cellulaire. Les données dans la littérature établissent un lien entre H3.3 et la transcription. L'incorporation d'H3.3 dépend d'une voie d'assemblage faisant intervenir le chaperon HIRA. Mon projet de recherche visait à déterminer si H3.3 et son incorporation via HIRA possédaient un rôle spécifique. Le développement embryonnaire via une régulation fine de l'expression des gènes représentait une situation idéale pour aborder ces questions. L'utilisation du vertébré Xenopus laevis qui ne possède qu'un variant H3 réplicatif : H3.2, m'a permis d'évaluer la fonction de ces variants au cours du développement. J'ai pu montrer que, malgré leur similarité, les variants H3.2 et H3.3 ne sont pas interchangeables. Une altération d'expression d'H3.3 ou l'interférence dans sa voie d'assemblage via son chaperon HIRA conduisent à des défauts majeurs à la gastrulation. Ce phénotype s'accompagne d'un défaut d'expression de gènes mésodermiques, dont le marqueur Xbra. Une désorganisation globale de la chromatine est également observée chez ces embryons. Ces données mettent en lumière l'importance de l'incorporation du variant d'histone H3.3 dans la chromatine au cours d'une étape clé du développement embryonnaire, la gastrulation

Schizophrenia may result from altered gene expression leading to abnormal neurodevelopment. In a search for genes with altered expression in schizophrenia, cDNA library subtractive hybridization experiments using post-mortem human frontal cerebral cortices from schizophrenia individuals and neurological controls were performed. I found the mRNA of two neurodevelopmentally important genes, Nogo (RTN4) and calcium/calmodulin-dependent protein kinase II beta (CaMKIIβ), to be overexpressed in post-mortem frontal cortex tissues from patients who suffered with schizophrenia. I used the quantitative real-time polymerase chain reaction method to determined the mRNA levels of these genes in tissues from age- and sex-matched individuals. Nogo is a myelin-associated protein which inhibits the outgrowth of neurites and nerve terminals. The gene produces three splice variants, Nogo-A, B and C. I found Nogo-C mRNA to be overexpressed by 26% in schizophrenia. I also found a 17% reduction of Nogo-B mRNA in samples from individuals who had been diagnosed with severe depression. Furthermore, I showed that there is a direct correlation between the expression of both Nogo-A and -C and the presence of a CAA insert in the 3’UTR of the Nogo gene. CaMKII is a kinase localized at the postsynaptic density. The holoenzyme is primarily composed of the subunits α and β, encoded by two separate genes. It influences the expression of many neuroreceptors, in particular receptors of the glutamatergic pathway. CaMKII also mediates neural maturation during puberty, a time of onset of schizophrenia. The expression of CaMKIIα was elevated 29% in frontal cortex tissues of patients who suffered from depression. The expression of CaMKIIβ was elevated 27% in tissues of schizophrenia patients and 36% in tissues of patients diagnosed with depression. Upregulation of CaMKIIβ was associated with the presence of the CAA insert in at least one copy of the Nogo gene in a group containing both healthy subjects and patients with mental illness, possibly linking the CaMKII and Nogo pathways. The values for the expression of Nogo, CaMKIIα and CaMKIIβ were normalized to β-glucuronidase expression to minimize the effects of mRNA degradation. These results confirm that upregulation of Nogo-C and CaMKIIβ is likely associated with schizophrenia.

<p><I> Trypanosoma congolense </i> is a single-cell blood parasite and an important pathogen causing African trypanosomiasis, also called ngana, in livestock. Ngana in cattle is a chronic disease associated with anemia, cachexia and increased susceptibility to secondary infections. Infection of mice can be used as an experimental model to study the host-parasite relationship. As determined by their survival time, BALB/c mice are highly susceptible to <i> T. congolense </i> infection, whereas C57BL/6 mice are relatively resistant. The surfaces of African trypanosomes are covered with a layer of a single species of glycoprotein, called variant surface glycoprotein (VSG). Production of antibodies to the VSG of African trypanosomes is one of the major immune responses leading to control of parasitemia. The reaction of antibodies with VSG of trypanosomes, for presently unknown reasons, predominantly activates the alternative complement pathway rather than the classical pathway of complement. IgM antibodies are the first and predominant class of anti-trypanosomal antibodies in infected animals. Antibody-mediated phagocytosis of <i> T. congolense </i> by macrophages is considered a major mechanism of control of parasitemia, besides antibody/complement-mediated lysis and cytotoxic effect by macrophage-derived nitric oxide (NO). The receptor(s) on macrophages that recognizes IgM antibody-coated trypanosomes and enables their phagocytosis is unknown. Interaction of antibodies with the VSG of trypanosomes not only causes phagocytosis of trypanosomes by macrophages, but also leads to the release of sVSG from the trypanosomes. sVSG has been found to modulate various functions of the host: induction of polyclonal B cell activation and modulation of macrophage functions, such as the induction of TNF-á synthesis and the inhibition of IFN-ã-induced nitric oxide production. The objectives of this thesis are:</p> <p> 1) to test whether CR3 (Mac-1; CD11b/18) is involved in IgM anti-VSG-mediated phagocytosis of <i> T. congolense </i> by macrophages </p> <p> 2) to test the effects of anti-VSG antibody and complement on the release of soluble VSG from <i> T. congolense </i> </p> <p>1) When the trypanosomes were incubated with IgM anti-VSG antibody and fresh mouse serum, fragments of complement component C3 were found to be deposited onto <i> Trypanosoma congolense </i>. Thus, it was assessed whether complement receptor CR3 (CD11b/CD18; receptor for iC3b) might be involved in IgM anti-VSG mediated phagocytosis of <i> T. congolense </i>. In the presence of fresh mouse serum, there was significantly and markedly less phagocytosis of IgM-opsonized <i> T. congolense </i> by CD11b-deficient macrophages compared to phagocytosis by normal macrophages (78% fewer <i> T. congolense </i> were ingested per macrophage). There also was significantly less TNF-á (38% less), but significantly more NO (63% more) secreted by CD11b-deficient macrophages that had engulfed trypanosomes than by equally treated normal macrophages. It was concluded that CR3 is the major, but not the only, receptor involved in IgM anti-VSG-mediated phagocytosis of <i> T. congolense </i> by macrophages. It was further concluded that signaling via CR3, associated with IgM anti-VSG-mediated phagocytosis of <i> T. congolense </i>, either directly or indirectly, enhances synthesis of disease-producing TNF-á and inhibits the synthesis of parasite-controlling NO.</p> <p> 2) This investigation revealed that there was more sVSG released from <i> T. congolense </i> by interaction with IgM anti-VSG than by interaction with equal amounts of IgG2a anti-VSG. The release of sVSG occurred in an antibody dose-dependent pattern. It was also found that IgM anti-VSG, after interacting with the surface of <i> T. congolense </i>, formed soluble immune complexes with released sVSG. The results also showed that antibody-induced release of sVSG can occur without complement, but is enhanced by complement. It was further tested whether fresh sera from either relatively resistant C57BL/6 mice or highly susceptible BALB/c mice, which differ in their complement cascade, had different effects on the release of sVSG from <i> T. congolense </i>. The results showed that antibody-induced shedding of sVSG was higher in the presence of fresh C57BL/6 serum than in the presence of fresh BALB/c serum. All these data suggest that the concentration of anti-VSG antibody, antibody class and source of complement can affect the release of sVSG from <i> T. congolense </i></p>.

A fixed terrestrial wireless system such as the Microwave Multi-channel Distribution Service (MMDS) can be used as the ``last mile' to provide a high speed Internet connection from a base station to a home in a rural or suburban residential area. Such a broadband wireless system works very well under line-of-sight transmission. It works quite well even if the line-of-sight is obstructed with a large number of trees. However, when trees obstruct the line-of-sight, under conditions of wind, the user may experience loss of the RF signal from time to time. This is especially true under gusty conditions. As part of this research a high precision DSP-based measuring system is devised to accurately measure and characterize the distortions caused by tree foliage on the RF line-of-sight signal. The approach is to digitally generate a signal composed of several tones, up-convert the signal to 2.5 GHz and send it through tree foliage to a receiver where the signal is down-converted and sampled for a duration of five seconds. The samples collected are processed using Matlab to compute the temporal amplitude and phase variations of the tones. The measurement system provides estimates of the amplitude and phase of the receive tones with a time resolution of 3.2 ms. The standard deviation of the amplitude estimates is 0.3\% of the actual amplitude of the tones and the standard deviation of the phase estimates is 0.23 degree. This accuracy is obtained when the signal-to-noise ratio of the receive signal is greater than 20 dB. Measurement in the field with tree foliage in the line-of-sight shows that the swaying of the branches in the wind can cause rapid signal fading. This research determines the type of fade, the depth and duration of the fade, as well as the fading rate.