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Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

Glioma is a unique neoplastic disease that develops exclusively in the central nervous system (CNS) and rarely metastasizes to other tissues. This feature strongly implicates the tumor-host CNS microenvironment in gliomagenesis and tumor progression. We investigated the differences and similarities in glioma biology as conveyed by transcriptomic patterns across four mammalian hosts: rats, mice, dogs, and humans. Given the inherent intra-tumoral molecular heterogeneity of human glioma, we focused this study on tumors with upregulation of the platelet-derived growth factor signaling axis, a common and early alteration in human gliomagenesis. The results reveal core neoplastic alterations in mammalian glioma, as well as unique contributions of the tumor host to neoplastic processes. Notable differences were observed in gene expression patterns as well as related biological pathways and cell populations known to mediate key elements of glioma biology, including angiogenesis, immune evasion, and brain invasion. These data provide new insights regarding mammalian models of human glioma, and how these insights and models relate to our current understanding of the human disease.

The identification and tracking of antigen-specific immunoglobulin (Ig) sequences within total Ig repertoires is central to high-throughput sequencing (HTS) studies of infections or vaccinations. In this context, public Ig sequences shared by different individuals exposed to the same antigen could be valuable markers for tracing back infections, measuring vaccine immunogenicity, and perhaps ultimately allow the reconstruction of the immunological history of an individual. Here, we immunized groups of transgenic rats expressing human Ig against tetanus toxoid (TT), Modified Vaccinia virus Ankara (MVA), measles virus hemagglutinin and fusion proteins expressed on MVA, and the environmental carcinogen benzo[a]pyrene, coupled to TT. We showed that these antigens impose a selective pressure causing the Ig heavy chain (IgH) repertoires of the rats to converge toward the expression of antibodies with highly similar IgH CDR3 amino acid sequences. We present a computational approach, similar to differential gene expression analysis, that selects for clusters of CDR3s with 80% similarity, significantly overrepresented within the different groups of immunized rats. These IgH clusters represent antigen-induced IgH signatures exhibiting stereotypic amino acid patterns including previously described TT- and measles-specific IgH sequences. Our data suggest that with the presented methodology, transgenic Ig rats can be utilized as a model to identify antigen-induced, human IgH signatures to a variety of different antigens.

The identification and tracking of antigen-specific immunoglobulin (Ig) sequences within total Ig repertoires is central to high-throughput sequencing (HTS) studies of infections or vaccinations. In this context, public Ig sequences shared by different individuals exposed to the same antigen could be valuable markers for tracing back infections, measuring vaccine immunogenicity, and perhaps ultimately allow the reconstruction of the immunological history of an individual. Here, we immunized groups of transgenic rats expressing human Ig against tetanus toxoid (TT), Modified Vaccinia virus Ankara (MVA), measles virus hemagglutinin and fusion proteins expressed on MVA, and the environmental carcinogen benzo[a]pyrene, coupled to TT. We showed that these antigens impose a selective pressure causing the Ig heavy chain (IgH) repertoires of the rats to converge toward the expression of antibodies with highly similar IgH CDR3 amino acid sequences. We present a computational approach, similar to differential gene expression analysis, that selects for clusters of CDR3s with 80% similarity, significantly overrepresented within the different groups of immunized rats. These IgH clusters represent antigen-induced IgH signatures exhibiting stereotypic amino acid patterns including previously described TT- and measles-specific IgH sequences. Our data suggest that with the presented methodology, transgenic Ig rats can be utilized as a model to identify antigen-induced, human IgH signatures to a variety of different antigens.

Tooth enamel is the hardest organ in the body. In rodent incisor, the enamel is exclusively produced by ameloblasts with yellowish-brown pigmentation, indicating normal enamel formation. However, the molecular mechanisms of ameloblast differentiation and amelogenesis are not fully understood. Specificity protein (Sp) 6 has been reported as one of the critical factors for tooth development. To explore SP6 function, we generated Sp6 transgenic (Tg) rats. Unexpectedly, the enamel surfaces of the incisors in Tg rats were discolored, even though enamel formation and serum iron concentrations were normal. Histological analysis of incisors from 6-week-old Tg rats demonstrated that the ameloblast layer at the pigmentation stage was elongated up to the gingival margin with ectopic SP6 expression in longitudinal incisor sections. In contrast, the incisors from 10-week-old Tg rats revealed that the pigmented ameloblasts were morphologically changed to those of the reduced stage, concomitant with the sporadic disappearance of ectopic SP6 expression. Here we report that morphological differentiation and metabolism of the iron-containing pigment in ameloblasts are independently regulated during amelogenesis by means of ectopic SP6 expression.

Die meisten Patienten mit hypertropher Kardiomyopathie und kongenitalen Herzerkrankungen exprimieren die atriale essentielle leichte Myosinkette (ALC-1) im Ventrikel, wo sie teilweise die ventrikuläre essentielle leichte Myosinkette (VLC-1) ersetzt. Diese VLC-1/ALC-1 Isoformveränderung korrelierte mit einem Anstieg der Zykluskinetik der Myosin-Querbrücken in chemisch gehäuteten Herzfasern aus hypertrophierten Humanventrikeln. Um die funktionelle Bedeutung der ALC-1 im gesamten intakten Herzen zu untersuchen, habe ich in der vorliegenden Arbeit ein transgenes Rattenmodell charakterisiert, das die humane ALC-1 (hALC-1) im Herzen exprimiert (TGR/hALC-1). WKY-Ratten dienten als genetisch korrekter Kontrollstamm. Mittels rekombinanter hALC-1 als Standard wurde die exprimierte hALC-1-Menge in SDS-Extrakten linker Ventrikel der TGR/hALC-1 im Western-Blot untersucht. 12 Wochen alte TGR/hALC-1 exprimierten etwa 17 mug hALC-1/mg SDS-Extrakt. Das exprimierte Transgen konnte in der Immunfluoreszenz zwischen den Z-Linien der Sarkomere lokalisiert werden. Die gerichtete Integrations des Transgens in das kardiale Myosinmolekül wurde zusätzlich noch in hochgereinigten Myosinpräparationen nachgewiesen. Analyse des linksventrikulären Proteoms durch 2D-PAGE, das zur Identifikation von etwa 3000 Proteinen führte, zeigte vergleichbare Proteinmuster in WKY und TGR/hALC-1. Die Untersuchungen der Kontraktilität des intakten isoliert perfundierten Herzen wurden mit Langendorff-Präparationen durchgeführt. Die Expression des hALC-1-Transgen führte zu statistisch signifikanten (p, Most patients with hypertrophic cardiomyopathy and congenital heart diseases express the atrial essential myosin light chains (ALC-1) in their ventricles, partially replacing the ventricular essential light chains (VLC-1). This VLC-1/ALC-1 isoform shift is correlated with an increase in cross-bridge cycling kinetics as measured using chemically skinned fibers from the hypertrophied ventricles of human hearts. To study the functional importance of hALC-1 in the whole intact perfused-heart, a transgenic rat model overexpressing hALC-1 (TGR/hALC-1) in the heart was generated. WKY rats were used as the respective genetically correct control strain. Using hALC-1HIST protein as a standard, the amount of transgenic protein expression was quantified by Immunoblot analysis of the left ventricular tissue extracts of the transgenic rats. Twelve-week-old TGR/hALC-1 expressed around 17mug hALC-1 per mg of whole SDS-soluble protein. The transgene was localized in-between the Z-lines of the sarcomere by immunofluoresecnce microscopy. Furthermore, the proper integration of the transgene into the rat ventricular myosin was confirmed by purifying myosin from rat ventricular tissues. Whole ventricular proteome analysis by 2D-PAGE, resolved approximately 3000 proteins spots in each TGR/hALC-1 and WKY animal. The whole protein expression patterns in both animal groups showed no differences with the exception of the transgenic hALC-1 protein spot. The perfused heart contractility parameters were evaluated using the Langendorff preparation. Expression of hALC-1 was accompanied by statistically significant improvements (p

Die meisten Patienten mit hypertropher Kardiomyopathie und kongenitalen Herzerkrankungen exprimieren die atriale essentielle leichte Myosinkette (ALC-1) im Ventrikel, wo sie teilweise die ventrikuläre essentielle leichte Myosinkette (VLC-1) ersetzt. Diese VLC-1/ALC-1 Isoformveränderung korrelierte mit einem Anstieg der Zykluskinetik der Myosin-Querbrücken in chemisch gehäuteten Herzfasern aus hypertrophierten Humanventrikeln. Um die funktionelle Bedeutung der ALC-1 im gesamten intakten Herzen zu untersuchen, habe ich in der vorliegenden Arbeit ein transgenes Rattenmodell charakterisiert, das die humane ALC-1 (hALC-1) im Herzen exprimiert (TGR/hALC-1). WKY-Ratten dienten als genetisch korrekter Kontrollstamm. Mittels rekombinanter hALC-1 als Standard wurde die exprimierte hALC-1-Menge in SDS-Extrakten linker Ventrikel der TGR/hALC-1 im Western-Blot untersucht. 12 Wochen alte TGR/hALC-1 exprimierten etwa 17 mug hALC-1/mg SDS-Extrakt. Das exprimierte Transgen konnte in der Immunfluoreszenz zwischen den Z-Linien der Sarkomere lokalisiert werden. Die gerichtete Integrations des Transgens in das kardiale Myosinmolekül wurde zusätzlich noch in hochgereinigten Myosinpräparationen nachgewiesen. Analyse des linksventrikulären Proteoms durch 2D-PAGE, das zur Identifikation von etwa 3000 Proteinen führte, zeigte vergleichbare Proteinmuster in WKY und TGR/hALC-1. Die Untersuchungen der Kontraktilität des intakten isoliert perfundierten Herzen wurden mit Langendorff-Präparationen durchgeführt. Die Expression des hALC-1-Transgen führte zu statistisch signifikanten (p, Most patients with hypertrophic cardiomyopathy and congenital heart diseases express the atrial essential myosin light chains (ALC-1) in their ventricles, partially replacing the ventricular essential light chains (VLC-1). This VLC-1/ALC-1 isoform shift is correlated with an increase in cross-bridge cycling kinetics as measured using chemically skinned fibers from the hypertrophied ventricles of human hearts. To study the functional importance of hALC-1 in the whole intact perfused-heart, a transgenic rat model overexpressing hALC-1 (TGR/hALC-1) in the heart was generated. WKY rats were used as the respective genetically correct control strain. Using hALC-1HIST protein as a standard, the amount of transgenic protein expression was quantified by Immunoblot analysis of the left ventricular tissue extracts of the transgenic rats. Twelve-week-old TGR/hALC-1 expressed around 17mug hALC-1 per mg of whole SDS-soluble protein. The transgene was localized in-between the Z-lines of the sarcomere by immunofluoresecnce microscopy. Furthermore, the proper integration of the transgene into the rat ventricular myosin was confirmed by purifying myosin from rat ventricular tissues. Whole ventricular proteome analysis by 2D-PAGE, resolved approximately 3000 proteins spots in each TGR/hALC-1 and WKY animal. The whole protein expression patterns in both animal groups showed no differences with the exception of the transgenic hALC-1 protein spot. The perfused heart contractility parameters were evaluated using the Langendorff preparation. Expression of hALC-1 was accompanied by statistically significant improvements (p

The development of a permissive small animal model for the study of human immunodeficiency virus type (HIV)-1 pathogenesis and the testing of antiviral strategies has been hampered by the inability of HIV-1 to infect primary rodent cells productively. In this study, we explored transgenic rats expressing the HIV-1 receptor complex as a susceptible host. Rats transgenic for human CD4 (hCD4) and the human chemokine receptor CCR5 (hCCR5) were generated that express the transgenes in CD4(+) T lymphocytes, macrophages, and microglia. In ex vivo cultures, CD4(+) T lymphocytes, macrophages, and microglia from hCD4/hCCR5 transgenic rats were highly susceptible to infection by HIV-1 R5 viruses leading to expression of abundant levels of early HIV-1 gene products comparable to those found in human reference cultures. Primary rat macrophages and microglia, but not lymphocytes, from double-transgenic rats could be productively infected by various recombinant and primary R5 strains of HIV-1. Moreover, after systemic challenge with HIV-1, lymphatic organs from hCD4/hCCR5 transgenic rats contained episomal 2-long terminal repeat (LTR) circles, integrated provirus, and early viral gene products, demonstrating susceptibility to HIV-1 in vivo. Transgenic rats also displayed a low-level plasma viremia early in infection. Thus, transgenic rats expressing the appropriate human receptor complex are promising candidates for a small animal model of HIV-1 infection.

The development of a permissive small animal model for the study of human immunodeficiency virus type (HIV)-1 pathogenesis and the testing of antiviral strategies has been hampered by the inability of HIV-1 to infect primary rodent cells productively. In this study, we explored transgenic rats expressing the HIV-1 receptor complex as a susceptible host. Rats transgenic for human CD4 (hCD4) and the human chemokine receptor CCR5 (hCCR5) were generated that express the transgenes in CD4(+) T lymphocytes, macrophages, and microglia. In ex vivo cultures, CD4(+) T lymphocytes, macrophages, and microglia from hCD4/hCCR5 transgenic rats were highly susceptible to infection by HIV-1 R5 viruses leading to expression of abundant levels of early HIV-1 gene products comparable to those found in human reference cultures. Primary rat macrophages and microglia, but not lymphocytes, from double-transgenic rats could be productively infected by various recombinant and primary R5 strains of HIV-1. Moreover, after systemic challenge with HIV-1, lymphatic organs from hCD4/hCCR5 transgenic rats contained episomal 2-long terminal repeat (LTR) circles, integrated provirus, and early viral gene products, demonstrating susceptibility to HIV-1 in vivo. Transgenic rats also displayed a low-level plasma viremia early in infection. Thus, transgenic rats expressing the appropriate human receptor complex are promising candidates for a small animal model of HIV-1 infection.

The objective of this study was to characterize events in the uniformly selective association of H-ras gene activation, but not K-ras gene activation, in the rat mammary carcinogenesis model. Three primary objectives were investigated. First, the relative tumorigenic potency of activated H-ras and K-ras-2B was investigated. The activated H-ras gene was found to be approximately 10-fold more potent at inducing mammary tumors than the activated K-ras gene. Yet, the K-ras oncogene was still effective at mammary carcinoma induction. Second, the relative percentage of mammary transplants with mutations in H-ras and K-ras was investigated. This objective will be completed soon, but, as yet, no data is available. The third objective was to investigate the role of H-ras regulatory elements in rat mammary tumorigenesis using transgenic rats harboring a H-ras gene (HrHr transgenics) or K-ras gene (HrKr transgenics) controlled by H-ras gene regulatory elements.

The objective of this study is to characterize cellular and molecular events of chemically induced rat mammary carcinogenesis by asking why is selective activation of the Harvey ras gene, but not other similar members of the ras gene family, associated with this model. This study is divided into three main objectives. First, the ability of the activated and wild-type forms df Harvey ras and Kirsten ras gene products was evaluated. Both oncogenes produced rat mammary tumors (therefore, excluding the possibility that Kirsten ras was not tumorigenic in the rat mammary gland), although the Harvey ras gene product was more tumorigenic. Second, the relative mutation frequency of Harvey ras and Kirsten ras genes in nitromethylurea exposed rat mammary clonogenic growths are currently being determined. Third, a transgenic rat model has been developed to evaluate the role of Harvey ras gene regulation. Five founder animals expressing multiple copies of the Harvey ras gene have been produced. In one group, E transgene has been observed to reduce tumor multiplicity following carcinogen exposure. Three founder transgenic animals expressing the Kirsten ras gene under Harvey ras - - regulatory elements have been produced and are under investigation.

Prítomnosť amyloidných plakov v hipokampuse upozorňuje na výskyt Alzheimerovej choroby. Manuálna segmentácia amyloidných plakov je veľmi časovo náročná a zvyšuje čas, ktorý môže byť využitý na sledovanie distribúcie amyloidných plakov. Distribúcia nesie významné informácie o progrese ochorenia a vplyvu potencionálnej terapie. Automatická alebo poloautomatická segmentačná metóda môže viesť ku značnému ušetreniu času, ktorý je pri rýchlom progrese choroby veľmi potrebný. Táto práca obsahuje popis amyloidných plakov a CT zobrazovacieho systému. V tejto diplomovej práci sú tri implementované algoritmy, dva z nich vychádzajú z publikovaných článkov a jeden je vlastné metodického riešenie. Záverom práce je kvantitatívne vyhodnotenie presnosti implementovaných segmentačných postupov., The presence of amyloid plaques in the hippocampus highlights the incidence of Alzheimer’s disease. Manual segmentation of amyloid plaques is very time consuming and increases the time that can be used to monitor the distribution of amyloid plaques. Distribution carries significant information about disease progression and the impact of potential therapy. The automatic or semi-automatic segmentation method can lead to significant savings in the time which are required when the disease has rapid progression. The description of amyloid plaques and the computed tomography are included in this work. In this diploma thesis are three implemented algorithms, two of them are based on published articles and one’s own methodological solution. The conclusion of the thesis is a quantitative evaluation of the accuracy of implemented segmentation procedures.

Prítomnosť amyloidných plakov v hipokampuse upozorňuje na výskyt Alzheimerovej choroby. Manuálna segmentácia amyloidných plakov je veľmi časovo náročná a zvyšuje čas, ktorý môže byť využitý na sledovanie distribúcie amyloidných plakov. Distribúcia nesie významné informácie o progrese ochorenia a vplyvu potencionálnej terapie. Automatická alebo poloautomatická segmentačná metóda môže viesť ku značnému ušetreniu času, ktorý je pri rýchlom progrese choroby veľmi potrebný. Táto práca obsahuje popis amyloidných plakov a CT zobrazovacieho systému. V tejto diplomovej práci sú tri implementované algoritmy, dva z nich vychádzajú z publikovaných článkov a jeden je vlastné metodického riešenie. Záverom práce je kvantitatívne vyhodnotenie presnosti implementovaných segmentačných postupov., The presence of amyloid plaques in the hippocampus highlights the incidence of Alzheimer’s disease. Manual segmentation of amyloid plaques is very time consuming and increases the time that can be used to monitor the distribution of amyloid plaques. Distribution carries significant information about disease progression and the impact of potential therapy. The automatic or semi-automatic segmentation method can lead to significant savings in the time which are required when the disease has rapid progression. The description of amyloid plaques and the computed tomography are included in this work. In this diploma thesis are three implemented algorithms, two of them are based on published articles and one’s own methodological solution. The conclusion of the thesis is a quantitative evaluation of the accuracy of implemented segmentation procedures.

Prítomnosť amyloidných plakov v hipokampuse upozorňuje na výskyt Alzheimerovej choroby. Manuálna segmentácia amyloidných plakov je veľmi časovo náročná a zvyšuje čas, ktorý môže byť využitý na sledovanie distribúcie amyloidných plakov. Distribúcia nesie významné informácie o progrese ochorenia a vplyvu potencionálnej terapie. Automatická alebo poloautomatická segmentačná metóda môže viesť ku značnému ušetreniu času, ktorý je pri rýchlom progrese choroby veľmi potrebný. Táto práca obsahuje popis amyloidných plakov a CT zobrazovacieho systému. V tejto diplomovej práci sú tri implementované algoritmy, dva z nich vychádzajú z publikovaných článkov a jeden je vlastné metodického riešenie. Záverom práce je kvantitatívne vyhodnotenie presnosti implementovaných segmentačných postupov., The presence of amyloid plaques in the hippocampus highlights the incidence of Alzheimer’s disease. Manual segmentation of amyloid plaques is very time consuming and increases the time that can be used to monitor the distribution of amyloid plaques. Distribution carries significant information about disease progression and the impact of potential therapy. The automatic or semi-automatic segmentation method can lead to significant savings in the time which are required when the disease has rapid progression. The description of amyloid plaques and the computed tomography are included in this work. In this diploma thesis are three implemented algorithms, two of them are based on published articles and one’s own methodological solution. The conclusion of the thesis is a quantitative evaluation of the accuracy of implemented segmentation procedures.

Prítomnosť amyloidných plakov v hipokampuse upozorňuje na výskyt Alzheimerovej choroby. Manuálna segmentácia amyloidných plakov je veľmi časovo náročná a zvyšuje čas, ktorý môže byť využitý na sledovanie distribúcie amyloidných plakov. Distribúcia nesie významné informácie o progrese ochorenia a vplyvu potencionálnej terapie. Automatická alebo poloautomatická segmentačná metóda môže viesť ku značnému ušetreniu času, ktorý je pri rýchlom progrese choroby veľmi potrebný. Táto práca obsahuje popis amyloidných plakov a CT zobrazovacieho systému. V tejto diplomovej práci sú tri implementované algoritmy, dva z nich vychádzajú z publikovaných článkov a jeden je vlastné metodického riešenie. Záverom práce je kvantitatívne vyhodnotenie presnosti implementovaných segmentačných postupov., The presence of amyloid plaques in the hippocampus highlights the incidence of Alzheimer’s disease. Manual segmentation of amyloid plaques is very time consuming and increases the time that can be used to monitor the distribution of amyloid plaques. Distribution carries significant information about disease progression and the impact of potential therapy. The automatic or semi-automatic segmentation method can lead to significant savings in the time which are required when the disease has rapid progression. The description of amyloid plaques and the computed tomography are included in this work. In this diploma thesis are three implemented algorithms, two of them are based on published articles and one’s own methodological solution. The conclusion of the thesis is a quantitative evaluation of the accuracy of implemented segmentation procedures.

Prítomnosť amyloidných plakov v hipokampuse upozorňuje na výskyt Alzheimerovej choroby. Manuálna segmentácia amyloidných plakov je veľmi časovo náročná a zvyšuje čas, ktorý môže byť využitý na sledovanie distribúcie amyloidných plakov. Distribúcia nesie významné informácie o progrese ochorenia a vplyvu potencionálnej terapie. Automatická alebo poloautomatická segmentačná metóda môže viesť ku značnému ušetreniu času, ktorý je pri rýchlom progrese choroby veľmi potrebný. Táto práca obsahuje popis amyloidných plakov a CT zobrazovacieho systému. V tejto diplomovej práci sú tri implementované algoritmy, dva z nich vychádzajú z publikovaných článkov a jeden je vlastné metodického riešenie. Záverom práce je kvantitatívne vyhodnotenie presnosti implementovaných segmentačných postupov., The presence of amyloid plaques in the hippocampus highlights the incidence of Alzheimer’s disease. Manual segmentation of amyloid plaques is very time consuming and increases the time that can be used to monitor the distribution of amyloid plaques. Distribution carries significant information about disease progression and the impact of potential therapy. The automatic or semi-automatic segmentation method can lead to significant savings in the time which are required when the disease has rapid progression. The description of amyloid plaques and the computed tomography are included in this work. In this diploma thesis are three implemented algorithms, two of them are based on published articles and one’s own methodological solution. The conclusion of the thesis is a quantitative evaluation of the accuracy of implemented segmentation procedures.