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.

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.

We develop a novel framework for optimized composition of explicitly parallel software components with different implementation variants given the problem size, data distribution scheme and processor group size on a Linux cluster. We consider two approaches (or two cases of the framework).  In the first approach, dispatch tables are built using measurement data obtained offline by executions for some (sample) points in the ranges of the context properties. Inter-/extrapolation is then used to do actual variant-selection for a given execution context at run-time. In the second approach, a cost function of each component variant is provided by the component writer for variant-selection. These cost functions can internally lookup measurements' tables built, either offline or at deployment time, for computation- and communication-specific primitives. In both approaches, the call to an explicitly parallel software component (with different implementation variants) is made via a dispatcher instead of calling a variant directly. As a case study, we apply both approaches on a parallel component for matrix multiplication with multiple implementation variants. We implemented our variants using Message Passing Interface (MPI). The results show the reduction in execution time for the optimally composed applications compared to applications with hard-coded composition. In addition, the results show the comparison of estimated and measured times for each variant using different data distributions, processor group and problem sizes.

<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>.

No description available.

<p>This Master’s thesis is aimed at improving the management of artifacts in the context of a joint-project between Jönköping University with the SEMCO project and industrial partner, a company involved in developing software for safety components. Both have a slightly distinct interest but this project can serve both parties.</p><p>Nowadays feature modelling is efficient way for domain analysis. The purpose of this master thesis is to analysis existing four popular feature diagrams, to find out commonalities between each of them and conclude results to give suggestions of how to use existing notation systems efficiently and according to situations.</p><p>The developed software based on knowledge established from research analysis. Two notation systems which are suggested in research part of the thesis report are implemented in the developed software “NotationManager”. The development procedures are also described and developer choices are mentioned along with the comparisons according to the situations</p><p>Scope of the research part as well as development is discussed. Future work for developed solution is also suggested.</p>

Genome-wide association studies (GWAS) have greatly improved our understanding of the genetic basis of complex traits. However, there are two major limitations with GWAS. First, most common variants identified by GWAS individually or in combination explain only a small proportion of heritability. This raises the possibility that additional forms of genetic variation, such as rare variants, could contribute to the missing heritability. The second limitation is that GWAS typically cannot identify which genes are being affected by the associated variants. Examination of rare variants, especially those in coding regions of the genome, can help address these issues. Moreover, several studies have recently identified low-frequency variants at both known and novel loci associated with complex traits, suggesting that functionally significant rare variants exist in the human population.

Innate immune signaling pathways initiate host defenses against viral pathogens. Receptors specific for viral nucleic acids activate these pathways culminating in cell-to-cell communication and/or cell death. In mammals, this cell- to-cell communication is achieved through the production of interferons and pro- inflammatory cytokines, which activate antiviral defenses in uninfected neighboring cells and instruct adaptive immune responses. The production of these signaling molecules is essential for the defense against viral infection, but must also be tightly regulated to prevent unnecessary inflammation. As an antiviral defense, cell death is also an effective mechanism to limit viral replication and spread but comes with the cost of tissue damage and inflammation. Therefore, regulating these antiviral responses is critical for controlling the spread of infection as well as preventing unnecessary pathologies related to excessive signaling. Hundreds of genes are involved in controlling these immune responses and a wide variety of mechanisms are utilized to regulate them. One mechanism to regulate gene function is the generation of protein variants through alternative translation. While polycistronic transcripts are a common feature of bacterial and viral gene expression, the process of alternative translation as a means to regulate gene function is not a feature generally attributed to mammalian mRNA. This dissertation describes a novel regulator of antiviral signaling that is generated through alternative translation. Expression of the transcript encoding the antiviral adaptor protein, MAVS, results in the production of two proteins: the full-length MAVS adaptor and a truncated variant, miniMAVS. Production of these proteins is in part regulated by cis-acting elements that control translation initiation. Production of miniMAVS regulates antiviral signaling by limiting interferon production induced by full-length MAVS, whereas both MAVS variants positively regulate cell death. To identify other examples of alternative translation in mammalian cells a genome-wide ribosomal profiling technique was used to generate a candidate list of antiviral truncation variants. This dissertation therefore demonstrates that protein variants generated through alternative translation of polycistronic mRNAs can be an effective mechanism for immune regulation and may be more common than previously understood.

The genetic structure of an intra-host viral population has an effect on many clinically important phenotypic traits such as escape from vaccine induced immunity, virulence, and response to antiviral therapies. Next-generation sequencing provides read-coverage sufficient for genomic reconstruction of a heterogeneous, yet highly similar, viral population; and more specifically, for the detection of rare variants. Admittedly, while depth is less of an issue for modern sequencers, the short length of generated reads complicates viral population assembly. This task is worsened by the presence of both random and systematic sequencing errors in huge amounts of data. In this dissertation I present completed work for reconstructing a viral population given next-generation sequencing data. Several algorithms are described for solving this problem under the error-free amplicon (or sliding-window) model. In order for these methods to handle actual real-world data, an error-correction method is proposed. A formal derivation of its likelihood model along with optimization steps for an EM algorithm are presented. Although these methods perform well, they cannot take into account paired-end sequencing data. In order to address this, a new method is detailed that works under the error-free paired-end case along with maximum a-posteriori estimation of the model parameters.

No description available.