No description available.

No description available.

<p>Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.</p>

Practicing clinical veterinarians in large companion animal practices are often faced with the phenomena of epileptic seizures which occur commonly in dogs. The high incidence of non-responsive cases is often frustrating, and the literature offers incomplete, conflicting and often inaccurate information. The concept of therapeutic anti-epileptic drug concentration monitoring, as applied in man as an aid to treatment, appears attractive in order to provide an improved service to the patient and client. An investigation into the pharmacokinetics of phenobarbitone, particularly at steady state, became necessary in order to interpret the application of drug serum concentration monitoring. The trend of veterinarians to extrapolate human kinetics to dogs is common and unsound. This study was an attempt to identify the similarities and dissimilarities between the pharmacokinetics of dogs and humans. No literature was available, both for man or animal, on the effect of food on the absorption of phenobarbitone. As dog owners frequently have to administer oral medication in food, this was an important factor to examine. The kinetics of the drug was determined in a group of epileptic dogs in order to provide a possible base-line therapeutic regime on commencement of treatment, and the practical application of therapeutic drug monitoring in order to individualize and improve response to treatment was explored. / Thesis (M.Sc.)-University of Durban-Westville, 1990.

No description available.

No description available.

<p>Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.</p>

Heart failure has a significant impact on mortality and morbidity. Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the most common reason for heart transplantation. Familial DCM is known to be caused by mutations in the LMNA gene encoding lamins A and C. New methods to enhance cardiac contractility would be beneficial in the treatment or prevention of heart failure. The focus of this thesis was to evaluate the mechanisms of altered contractility in two mouse models: the LMNA knockout model (homozygous, Lmna-/-; heterozygous, Lmna+/-) generated by targeted deletion of the lmna gene, and the model of enhanced contractility due to cardiac alpha1A-adrenergic receptor (???1A-AR) overexpression (A1A1). Previous studies have found altered nuclear-desmin connections in lamin A/C deficient mice. It was proposed that these alterations result in ???defective force transmission???, which leads to DCM. Studies in this thesis have supported this hypothesis. Studies of isolated single cardiomyocytes from mice aged 4-6 weeks demonstrated abnormal cell morphology and contractile dysfunction in Lmna-/- cardiomyocytes, while Lmna+/- cells showed no overt phenotype. Excitation-contraction coupling experiments and forcecalcium studies in skinned fibers excluded altered calcium kinetics as a primary cause of DCM in this model, but there was evidence of reduced sarcomere numbers and reduced sarcomere lengths as a contributor to reduce force generation in Lmna-/- and Lmna+/- mice. Previous in vivo studies showed that A1A1 mice had enhanced contractility with the absence of hypertrophy. Studies on isolated single cardiomyocytes from A1A1 mice aged 8-12 weeks showed reduced contractility in the absence of ???1A-AR stimulation, but an exaggerated response to ???1A-AR stimulation. In contrast isolated isovolumic Langendorff perfused A1A1 hearts without ???1A-AR stimulation replicated the enhanced contractility observed in vivo. These studies are consistent with down-regulation of contractility due to the hyperactivity of the overexpressed ???1A-AR in vivo, which only becomes evident in isolated cells without ???1A-AR stimulation due to the loss of functional receptor numbers during isolation. Sufficient spontaneously active ???1A-ARs are preserved in the isolated Langendorff heart preparation to ensure maximum contractility driven by increase calcium release.

Contact Lens Acute Red Eye (CLARE) and Infiltrative Keratitis (IK) are inflammatory responses of the eye associated with extended wear of soft contact lenses. Bacterial colonization of contact lenses with Gram-negative bacteria such as Pseudomonas aeruginosa is an important risk factor for the development of these adverse responses. Strategies that control the bacterial colonization of contact lenses may help prevent the occurrence of adverse responses. This thesis aimed to develop an animal model of CLARE/IK to test this hypothesis and to test the effectiveness of contact lenses containing antimicrobial compounds, namely silver and furanone compounds, in controlling corneal inflammation caused by Pseudomonas aeruginosa. A guinea pig model of contact lens wear was developed for the study and it was observed that the ocular responses to contact lens wear in the guinea pig were similar to those seen in human eyes wearing contact lenses. Also, three different models for CLARE/IK were developed and tested in the guinea pig eye. The pathological features of CLARE/IK in the guinea pig were virtually identical to those observed in human eyes. Bacterial contamination of contact lenses was confirmed to be a major risk factor for the development of CLARE/IK. Contact lenses containing nano-particles of silver demonstrated very good antibacterial activity against Pseudomonas aeruginosa in-vitro. The silver lenses were able to control the development of CLARE/IK responses in one of the models for CLARE/IK. Silver lenses might be most effective if used to prevent the establishment of a biofilm of bacteria on a lens such as might occur during storage in a contact lens case. Contact lenses were coated with different concentrations of the furanone compounds by physical adsorption and demonstrated good antibacterial activity at higher concentrations. However these concentrations were cytotoxic in-vitro and lower concentrations of furanones did not possess adequate antibacterial activity to control CLARE/IK responses in-vivo. This thesis has successfully demonstrated that guinea pigs can be used to test the effects of extended wear of contact lenses and developed models to test the pathogenesis of adverse responses such as CLARE/IK. The CLARE/IK models developed could be used to further our understanding of the pathogenesis of these inflammatory conditions and explore the activity of other antimicrobials.

Thesis (M.S.)--University of North Carolina Wilmington, 2007. / Includes bibliographical references (Leaves: 37-44)