Thesis (M.Med.Sc.)--University of Hong Kong, 1986. / Also available in print.

Orientador: Alexandre Secorun Borges / Banca: Rogerio Martins Amorim / Banca: Sandra Regina Torelli / Resumo: O intuito deste estudo foi determinar se os sinais neurológicos apresentados por cães com suspeita de neoplasia intracraniana foram compatíveis com a localização anatômica do tumor determinada com a utilização da tomografia computadorizada. Foram estudados 20 cães submetidos a avaliação neurológica e exame tomográfico encefálico. Estes cães foram divididos em 3 grupos de acordo com a área anatômica envolvida. Grupo I (n=14) animais com lesão em telencéfalo, diencéfalo e síndrome cerebral. Grupo II (n=4) lesão em tronco encefálico e cerebelo com síndrome cerebelar e de tronco encefálico. Grupo III (n=2) cães com lesão em diencéfalo compatível com tumor hipofisário apresentando síndrome cerebral. Aproximadamente 65% dos cães apresentaram sinais neurológicos compatíveis com a localização da lesão tumoral, evidenciada na tomografia. Nos outros animais (35%) todos pertencentes do grupo I foram observados sinais clínicos não associados à lesão tumoral primária estando provavelmente associados aos efeitos secundários decorrentes da lesão, tais como edema peritumoral, hemorragia, hidrocefalia, aumento de pressão intracraniana, processos inflamatórios dentre outros / Abstract: The purpose of this study was to determine if neurological signs shown by dogs with suspected intracranial neoplasm were consistent with the anatomical location of the tumor determined using computed tomography. We studied 20 dogs underwent neurological evaluation and brain CT scan. These dogs were divided into three groups according to the anatomic area involved. Group I (n = 14) animals with lesions in the telencephalon, diencephalon and brain syndrome. Group II (n = 4) lesion in brain stem and cerebellum with cerebellar syndrome and brainstem. Group III (n = 2) in dogs with injuries consistent with diencephalon pituitary tumor presenting brain syndrome. Approximately 65% of dogs had neurologic signs consistent with the location of the tumor, shown on CT. In other animals (35%) all belonging to group I showed no clinical signs associated with primary tumor and is probably associated with side effects resulting from injury, such as peritumoral edema, hemorrhage, hydrocephalus, increased intracranial pressure, inflammatory processes and others / Mestre

Made available in DSpace on 2014-06-11T19:27:15Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-08-13Bitstream added on 2014-06-13T20:16:18Z : No. of bitstreams: 1 jimenez_cd_me_botfmvz.pdf: 2023223 bytes, checksum: 0d707644d193ee36e94427b90363ca22 (MD5) / Universidade Estadual Paulista (UNESP) / O intuito deste estudo foi determinar se os sinais neurológicos apresentados por cães com suspeita de neoplasia intracraniana foram compatíveis com a localização anatômica do tumor determinada com a utilização da tomografia computadorizada. Foram estudados 20 cães submetidos a avaliação neurológica e exame tomográfico encefálico. Estes cães foram divididos em 3 grupos de acordo com a área anatômica envolvida. Grupo I (n=14) animais com lesão em telencéfalo, diencéfalo e síndrome cerebral. Grupo II (n=4) lesão em tronco encefálico e cerebelo com síndrome cerebelar e de tronco encefálico. Grupo III (n=2) cães com lesão em diencéfalo compatível com tumor hipofisário apresentando síndrome cerebral. Aproximadamente 65% dos cães apresentaram sinais neurológicos compatíveis com a localização da lesão tumoral, evidenciada na tomografia. Nos outros animais (35%) todos pertencentes do grupo I foram observados sinais clínicos não associados à lesão tumoral primária estando provavelmente associados aos efeitos secundários decorrentes da lesão, tais como edema peritumoral, hemorragia, hidrocefalia, aumento de pressão intracraniana, processos inflamatórios dentre outros / The purpose of this study was to determine if neurological signs shown by dogs with suspected intracranial neoplasm were consistent with the anatomical location of the tumor determined using computed tomography. We studied 20 dogs underwent neurological evaluation and brain CT scan. These dogs were divided into three groups according to the anatomic area involved. Group I (n = 14) animals with lesions in the telencephalon, diencephalon and brain syndrome. Group II (n = 4) lesion in brain stem and cerebellum with cerebellar syndrome and brainstem. Group III (n = 2) in dogs with injuries consistent with diencephalon pituitary tumor presenting brain syndrome. Approximately 65% of dogs had neurologic signs consistent with the location of the tumor, shown on CT. In other animals (35%) all belonging to group I showed no clinical signs associated with primary tumor and is probably associated with side effects resulting from injury, such as peritumoral edema, hemorrhage, hydrocephalus, increased intracranial pressure, inflammatory processes and others

Thesis (Master Diploma (Medical Technology) -- Cape Technikon, Cape Town, 1992 / The steady state in a tumour rapidly changes with its growth and the subsequent deteriorating blood and nutrient supply. This adaptation in the steady state of the tumour is shown in the increased lactate dehydrogenase and acid phosphatase activity in the tumour during it's growth. These alterations in the tumour metabolism places an increased burden on the body to supply nutrient and to discard the waste products of the tumour. This is demonstrated at the macroscopic level by the decreasing body weight and food intake when the tumour burden increases, and also at the metabolic levels by the responses of certain glycolytic and Cori cycle enzymes. Furthermore three distinct stages were observed in the Corl cycle response to the influence of the tumour namely, a silent or preclinical stage, a hypermetabolic stage and a hypometabolic stage. Although the decreasing body weight cannot be directly linked to the process of gluconeogenesis, the onset of anorexia appeared to coincide with the end of the hypermetabolic stage and the beginning of the hypometabolic stage in gluconeogenesis. This clearly shows that the body's steady state is adversely affected by the presence of the tumour and that the conditions at the metabolic level seem to cause the anorexia. Furthermore, it is well known that the success of cancer therapies depends entirely on the effectiveness o{the modality to kill the tumour cell and on the ability . of the host to absorb the damage caused by the modality without being destroyed in the process itself. The second part of this study demonstrates the radioprotective effects of ATP at all levels. It is clear from this work that ATP had a bigger influence in protecting the normal tissue than it had on the tumour tissue. This was demonstrated by the response of acid phosphatase (AP) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the tumour and testis. Furthermore, it would seem that ATP has a multifactorial interaction with the cell, two possible mechanisms of protection are indicated by these results. The fIrst of these interactions is through the receptors of the cell to stimulate enhanced glycolysis, for higher energy production and thus repair. The second possibility is the interaction of ATP with the receptor of the cell to inhibit the production of free radicals and thus damage, as demonstrated by the response of G-6-PDH and AP.

Thesis (BTech (Biomedical Technology))--Cape Technikon, 1992. / The steady state in a tumour rapidly changes with its growth and the subsequent deteriorating blood and nutrient supply. This adaptation in the steady state of the tumour is shown in the increased lactate dehydrogenase and acid phosphatase activity in the tumour during it's growth. These alterations in the tumour metabolism places an increased burden on the body to supply nutrient and to discard the waste products of the tumour. This is demonstrated at the macroscopic level by the decreasing body weight and food intake when the tumour burden increases, and also at the metabolic levels by the responses of certain glycolytic and Cori cycle enzymes. Furthermore three distinct stages were observed in the Cori cycle response to the influence of the tumour namely, a silent or preclinical stage, a hypermetabolic stage and a hypo metabolic stage. Although the decreasing body weight cannot be directly linked to the process of gluconeogenesis, the onset of anorexia appeared to coincide with the end of the hypermetabolic stage and the beginning of the hypometabolic stage in gluconeogenesis. This clearly shows that the body's steady state is adversely affected by the presence of the tumour and that the conditions at the metabolic level seem to cause the anorexia. Furthermore, it is well known that the success of cancer therapies depends entirely on the effectiveness ofthe modality to kill the tumour cell and on the ability' of the host to absorb the damage caused by the modality without being destroyed in the process itself. The second part of this study demonstrates the radioprotective effects of ATP at all levels. It is clear from this work that ATP had a bigger influence in protecting the normal tissue than it had on the tumour tissue. This was demonstrated by the response of acid phosphatase (AP) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the tumour and testis. Furthermore, it would seem that ATP has a multifactorial interaction with the cell, two possible mechanisms of protection are indicated by these results. The first of these interactions is through the receptors of the cell to stimulate enhanced glycolysis, for higher energy production and thus repair. The second possibility is the interaction of ATP with the receptor of the cell to inhibit the production of free radicals and thus damage, as demonstrated by the response of G-6-PDH and AP.

Thesis (MTech (Medical Technology))--Cape Technikon, 1992. / The steady state in a tumour rapidly changes with its growth and the subsequent deteriorating blood and nutrient supply. This adaptation in the steady state of the tumour is shown in the increased lactate dehydrogenase and acid phosphatase activity in the tumour during it's growth. These alterations in the tumour metabolism places an increased burden on the body to supply nutrient and to discard the waste products of the tumour. This is demonstrated at the macroscopic level by the decreasing body weight and food intake when the tumour burden increases, and also at the metabolic levels by the responses of certain glycolytic and Cori cycle enzymes. Furthermore three distinct stages were observed in the Cori cycle response to the influence of the tumour namely, a silent or preclinical stage, a hypermetabolic stage and a hypometabolic stage. Although the decreasing body weight cannot be directly linked to the process of gluconeogenesis, the onset of anorexia appeared to coincide with the end of the hypermetabolic stage and the beginning of the hypometabolic stage in gluconeogenesis. This clearly shows that the body's steady state is adversely affected by the presence of the tumour and that the conditions at the metabolic level seem to cause the anorexia. Furthermore, it is well known that the success of cancer therapies depends entirely on the effectiveness of the modality to kill the tumour cell and on the ability' of the host to absorb the damage caused by the modality without being destroyed in the process itself. The second part of this study demonstrates the radioprotective effects of ATP at all levels. It is clear from this work that ATP had a bigger influence in protecting the normal tissue than it had on the tumour tissue. This was demonstrated by the response of acid phosphatase (AP) and glucose-ó-phosphate dehydrogenase (G-6-PDH) in the tumour and testis. Furthermore, it would seem that ATP has a multifactorial interaction with the cell, two possible mechanisms of protection are indicated by these results. The first of these interactions is through the receptors of the cell to stimulate enhanced glycolysis, for higher energy production and thus repair. The second possibility is the interaction of ATP with the receptor of the cell to inhibit the production of free radicals and thus damage, as demonstrated by the response of G-6-PDH and AP.

Mouse mammary tumor is a common form of cancer used for experimental purposes. It is relatively resistant to chemotherapy. This investigation is designed to test the effect of heparin, a naturally occurring anticoagulant, on tumor growth using a genetically uniform laboratory animal.

M.S.

Thesis (Ph.D.)--Victoria University of Wellington, 2009. / Includes bibliographical references.

Thesis (M.S.)--Brigham Young University. Dept. of Microbiology and Molecular Biology, 2006. / Includes bibliographical references (p. 42-43).