The purpose of this investigation was to compare the frequencies of normal and abnormal findings from exercise electrocardiography (ECG), post-exercise echocardiography (ECHO) and angiography studies in a series of hypertensive and normotensive individuals who underwent diagnostic testing. Data for the ECG and ECHO were obtained simultaneously and the angiography was performed either before or following the exercise stress test. Thirty-seven cases were included in this retrospective study. Records were excluded if patients had: history of myocardial infarction; valvular heart disease; ECG evidence of abnormal Q waves, left ventricular hypertrophy (LVH) with abnormal ST/T wave pattern, or left bundle branch block (LBBB); medications that would alter blood pressure responses or ECG interpretation, technically uninterpretable records; or failure to attain 85% of age-adjusted maximal heart rates during the exercise tests. Subjects were defined as hypertensive (HYP) if at least two of the following criteria were met: 1) SBP ≥ 140 mmHg or DBP ≥ 90 mmHg; 2) current use of antihypertensive medications; or 3) history of hypertension. Normotensive subjects (NORM) were defined as absence of the above criteria. Data for the ECG and ECHO variables were obtained simultaneously in association with treadmill exercise studies. In each test, ECG measures were taken at peak exercise while the ECHO data were taken within 90 seconds immediately post exercise to obtain images. ECG response was considered abnormal if the ST shifted ≥ .1 mV from baseline at J₆₀ , while the ECHO response was considered abnormal when new or worsening of pre-existing wall motion abnormalities was observed. The 2-D ECHO's were recorded with the subject in the left lateral decubitus position, and parasternal long- and short-axis apical two and four chamber views were recorded for qualitative determination of wall motion abnormalities. Eleven of the 37 subjects also underwent angiography. Chi-square analysis demonstrated that high blood pressure status did not increase the frequency of abnormal test results for the ECHO (Χ²= 0.00009, DF = 1, p>.05), the exercise ECG (Χ²= 0.07, DF = 1, p>.05) nor for the angiography (Χ²= 0.69, DF = 1, p>.05). These results indicate that resting blood pressure does not influence the occurrence of abnormal vs normal ECG and ECHO findings nor angiography findings between hypertensive and normotensive subjects. There was also no significant differences between the ECG and ECHO in the occurrence of abnormal findings for NORM subjects (Χ²=2.43E-015, DF = 1, p>.05) nor HYP subjects (Χ²=0.13, DF = 1, p>.05). The ECHO showed 80% true-positive findings and the ECG showed 60% compared to the angiography. Both the ECG and ECHO had the same percentage of true-negatives (33%) compared to the angiography results. Since there was a higher percentage of ECHO true-positive results compared to the angiography then the ECG, this may indicate that the ECHO is comparable to the angiography findings and may be a better predictor in determining disease than the ECG. However, these data warrant further evaluation studies. / Master of Science

Cardiovascular disease and cancer are the two most common causes of death worldwide. Angiogenesis plays a critical role tumourigenesis and atherogenesis. As a member of the basic region-leucine zipper protein family, c-Jun, has been linked with cell proliferation, migration and cell survival. However, the relationship between c-Jun and angiogenesis has not been firmly established. In this thesis, strategies targeting c-Jun mRNA such as DNAzyme and siRNA have been designed and evaluated for their ability to inhibit the c-Jun mRNA and c-Jun protein expression in vitro and in vivo. These agents block c-Jun expression and inhibit DNA binding activity of c-Jun. Luciferase assay showed that c-Jun siRNA suppressed c-Jun/AP-1-dependent reporter activity. The processes of cell proliferation, migration, invasion and tube formation were all down-regulated after treatment with c-Jun targeting agents. In vivo, c-Jun DNAzymes and siRNA inhibit angiogenesis in multiple models of angiogenesis in multiple models of angiogenesis, including tumour angiogenesis and growth, matrix angiogenesis, corneal angiogenesis and retinal neovascularization. This is mediated, at least in part, by c-Jun siRNA or DNAzyme inhibition of MMP-2 expression. These findings demonstrate the critical role played by c-Jun in the involvement of neovascularization and suggest that DNAzymes or siRNAs are efficient gene-silencing agents. The ability to identify and control key genes in angiogenesis provides opportunities for developing therapeutic molecular tools to treat cancer or other angiogenesis related diseases.

The objective of this work is to improve the diagnostic quality and reduce the radiation dose of computed tomography coronary angiography (CTCA) imaging by developing gating techniques based on signals derived from cardiac motion, rather than the currently used electrocardiogram (ECG), to more reliably trigger data acquisition during periods of cardiac quiescence. Because the ECG is an indication of electrical activity, it is a surrogate marker of the mechanical state of the heart. Therefore, gating based on a signal derived directly from cardiac motion using either echocardiography or seismocardiography (SCG) should prove better at detecting and predicting periods of cardiac quiescence. Improved gating would permit the use of CTCA in more instances to either replace or determine the necessity of invasive and expensive CCAs. This work presents novel methods for detecting and predicting cardiac quiescence. Quiescence is detected as periods of minimal velocity from echocardiography, computed tomography (CT), and SCG. Identified quiescent periods are used to develop and evaluate techniques for predicting cardiac quiescence using echocardiography and SCG. Both echocardiography and SCG are shown to be more accurate for predicting quiescent periods than ECG. Additionally, the average motion during quiescent periods predicted by echocardiography and SCG is shown to be lower than those predicted using only ECG. Lastly, cardiac CT reconstructions from quiescent phases predicted by a commercial CT scanner were compared to the optimal quiescent phases calculated using the CT quiescence detection methods presented in this work. The diagnostic quality of the reconstructions from the optimal phases was found to be higher than that of the phases predicted by the CT scanner, suggesting that there is the potential for marked improvement in CTCA performance through more accurate cardiac gating.

Cardiovascular disease and cancer are the two most common causes of death worldwide. Angiogenesis plays a critical role tumourigenesis and atherogenesis. As a member of the basic region-leucine zipper protein family, c-Jun, has been linked with cell proliferation, migration and cell survival. However, the relationship between c-Jun and angiogenesis has not been firmly established. In this thesis, strategies targeting c-Jun mRNA such as DNAzyme and siRNA have been designed and evaluated for their ability to inhibit the c-Jun mRNA and c-Jun protein expression in vitro and in vivo. These agents block c-Jun expression and inhibit DNA binding activity of c-Jun. Luciferase assay showed that c-Jun siRNA suppressed c-Jun/AP-1-dependent reporter activity. The processes of cell proliferation, migration, invasion and tube formation were all down-regulated after treatment with c-Jun targeting agents. In vivo, c-Jun DNAzymes and siRNA inhibit angiogenesis in multiple models of angiogenesis in multiple models of angiogenesis, including tumour angiogenesis and growth, matrix angiogenesis, corneal angiogenesis and retinal neovascularization. This is mediated, at least in part, by c-Jun siRNA or DNAzyme inhibition of MMP-2 expression. These findings demonstrate the critical role played by c-Jun in the involvement of neovascularization and suggest that DNAzymes or siRNAs are efficient gene-silencing agents. The ability to identify and control key genes in angiogenesis provides opportunities for developing therapeutic molecular tools to treat cancer or other angiogenesis related diseases.

Cardiovascular disease and cancer are the two most common causes of death worldwide. Angiogenesis plays a critical role tumourigenesis and atherogenesis. As a member of the basic region-leucine zipper protein family, c-Jun, has been linked with cell proliferation, migration and cell survival. However, the relationship between c-Jun and angiogenesis has not been firmly established. In this thesis, strategies targeting c-Jun mRNA such as DNAzyme and siRNA have been designed and evaluated for their ability to inhibit the c-Jun mRNA and c-Jun protein expression in vitro and in vivo. These agents block c-Jun expression and inhibit DNA binding activity of c-Jun. Luciferase assay showed that c-Jun siRNA suppressed c-Jun/AP-1-dependent reporter activity. The processes of cell proliferation, migration, invasion and tube formation were all down-regulated after treatment with c-Jun targeting agents. In vivo, c-Jun DNAzymes and siRNA inhibit angiogenesis in multiple models of angiogenesis in multiple models of angiogenesis, including tumour angiogenesis and growth, matrix angiogenesis, corneal angiogenesis and retinal neovascularization. This is mediated, at least in part, by c-Jun siRNA or DNAzyme inhibition of MMP-2 expression. These findings demonstrate the critical role played by c-Jun in the involvement of neovascularization and suggest that DNAzymes or siRNAs are efficient gene-silencing agents. The ability to identify and control key genes in angiogenesis provides opportunities for developing therapeutic molecular tools to treat cancer or other angiogenesis related diseases.

Cardiovascular disease and cancer are the two most common causes of death worldwide. Angiogenesis plays a critical role tumourigenesis and atherogenesis. As a member of the basic region-leucine zipper protein family, c-Jun, has been linked with cell proliferation, migration and cell survival. However, the relationship between c-Jun and angiogenesis has not been firmly established. In this thesis, strategies targeting c-Jun mRNA such as DNAzyme and siRNA have been designed and evaluated for their ability to inhibit the c-Jun mRNA and c-Jun protein expression in vitro and in vivo. These agents block c-Jun expression and inhibit DNA binding activity of c-Jun. Luciferase assay showed that c-Jun siRNA suppressed c-Jun/AP-1-dependent reporter activity. The processes of cell proliferation, migration, invasion and tube formation were all down-regulated after treatment with c-Jun targeting agents. In vivo, c-Jun DNAzymes and siRNA inhibit angiogenesis in multiple models of angiogenesis in multiple models of angiogenesis, including tumour angiogenesis and growth, matrix angiogenesis, corneal angiogenesis and retinal neovascularization. This is mediated, at least in part, by c-Jun siRNA or DNAzyme inhibition of MMP-2 expression. These findings demonstrate the critical role played by c-Jun in the involvement of neovascularization and suggest that DNAzymes or siRNAs are efficient gene-silencing agents. The ability to identify and control key genes in angiogenesis provides opportunities for developing therapeutic molecular tools to treat cancer or other angiogenesis related diseases.

Cardiovascular disease and cancer are the two most common causes of death worldwide. Angiogenesis plays a critical role tumourigenesis and atherogenesis. As a member of the basic region-leucine zipper protein family, c-Jun, has been linked with cell proliferation, migration and cell survival. However, the relationship between c-Jun and angiogenesis has not been firmly established. In this thesis, strategies targeting c-Jun mRNA such as DNAzyme and siRNA have been designed and evaluated for their ability to inhibit the c-Jun mRNA and c-Jun protein expression in vitro and in vivo. These agents block c-Jun expression and inhibit DNA binding activity of c-Jun. Luciferase assay showed that c-Jun siRNA suppressed c-Jun/AP-1-dependent reporter activity. The processes of cell proliferation, migration, invasion and tube formation were all down-regulated after treatment with c-Jun targeting agents. In vivo, c-Jun DNAzymes and siRNA inhibit angiogenesis in multiple models of angiogenesis in multiple models of angiogenesis, including tumour angiogenesis and growth, matrix angiogenesis, corneal angiogenesis and retinal neovascularization. This is mediated, at least in part, by c-Jun siRNA or DNAzyme inhibition of MMP-2 expression. These findings demonstrate the critical role played by c-Jun in the involvement of neovascularization and suggest that DNAzymes or siRNAs are efficient gene-silencing agents. The ability to identify and control key genes in angiogenesis provides opportunities for developing therapeutic molecular tools to treat cancer or other angiogenesis related diseases.

Thesis (M. P. H.)--University of Hong Kong, 2007.

Thesis (M. P. H.)--University of Hong Kong, 2007. / Also available in print.

In addition all patients examined by means of using testicular angiography before the first of November 1978» have been included. 123 patients were intended for angiography, 13 of them bilaterally. The intention with the investigation was to determine whether selective angiography of the testicular artery might be a useful examination in cases of a non-palpable testis and in patients with different intrascrotal lesions. There is a description of a useful method of investigation. The normal angiographic anatomy of the testicular artery is also de­scribed, both retroperitoneally and in the scrotum. In cases with a non-palpable testis it is shown that it is easy to distinguish between agenesis and cryptorchism. The normal magnification angiography of the testis is shown and how various intrascrotal lesions alter the picture. Finally some cases with retroperitoneal lesions are presented in which the testicular artery is committed. / <p>Diss. Umeå : Umeå universitet, 1979, härtill 4 uppsatser</p> / digitalisering@umu