Le but de l'étude était de comparer l'étendue de mouvement passif de la hanche, les moments de force et l'endurance des ischio-jambiers et des adducteurs de la hanche de gardiens de but et de joueurs durant une saison de hockey sur glace. Les paramètres de la condition physique musculaire indiqués précédemment furent mesurés à trois reprises durant la saison de hockey chez huit gardiens de but et quatorze joueurs. L'étendue de mouvement passif de la hanche fut mesurée dans le plan sagittal et frontal. Les moments de force concentriques, excentriques et isométriques des deux groupes musculaires furent mesurés à l'aide d'un appareil isocinétique (Kin Com, 500H, Chattanooga, TN, USA). L'endurance isométrique des deux groupes musculaires fut mesurée en maintenant 85% de la charge maximale isométrique le plus longtemps possible jusqu'à 60s pendant que l'activité électromyographique était enregistrée. Les résultats démontrèrent que les gardiens de but avaient une meilleure étendue de mouvement passif de la hanche que les joueurs dans le plan sagittal (gardiens de but 104.7°, joueurs 91.9°) ainsi que dans le plan frontal (gardiens de but 37.7°, joueurs 31.7°). Certaines différences mineures entre les deux groupes de participants fut remarquées en ce qui a trait aux moments de force concentriques, excentriques et isométriques des deux groupes musculaires étudiés sans être significative. Au niveau de l'endurance musculaire isométrique des ischio-jambiers, les résultats démontrèrent une baisse plus importante en pourcentage de la fréquence médiane des ischio-jambiers chez les gardiens de but pour la session 1 et 3 (BF: 24.6% et 32.2%. ST: 24.3% et 42.2%) comparativement aux joueurs (BF: 16.8% et 19.5%. ST: 27.6% et 27.9%). Les conclusions de cette étude sous-entendraient que les gardiens de but posséderaient une étendue de mouvement passif de la hanche supérieure aux joueurs tant au plan sagittal que frontal. Les deux groupes posséderaient des moments de force comparables entre eux. Cependant, les gardiens de but se fatigueraient plus rapidement au niveau des ischio-jambiers que les joueurs.

The purpose of this study was to describe the functional role of the lower limb musculature during stationary cycling using electromyography, muscle-tendon unit length changes, and segmental kinematics. Five subjects were filmed (100 Hz) in synchrony with the collection of LE EMG activity of the gluteus maximus, semitendinosus, semimembranosus, rectus femoris, vastus lateralis, soleus, gastrocnemius, and tibialis anterior muscles during stationary cycling at 160 W (90 r/min). The results showed that extension during the propulsive phase of the pedal cycle was the result of high concentric activity of both the monoarticular and biarticular muscles. Furthermore, these muscles functioned according to their expected anatomical roles (Rasch and Burke, 1978). This investigation, therefore, finds little evidence for the existence of paradoxical muscle function as hypothesized by Lombard (1903), Molbech (1965), or Rasch & Burke (1978).

In filming and digitizing human segmental motion, external markers do not necessarily represent a true picture of the actual bone movement. When surface markers are placed on the skin or skate boot (in ice hockey) they move according to skin or boot movement, which does not exactly match bone movement. This results in a misrepresentation of the joint axes of rotation and a greater margin of error in motion measurement and analysis. This problem occurs for ankle and foot movements as their motion is quantified about the ankle joint complex (talocrural and subtalar joints). Hockey skates are vastly more rigid than regular shoes and their restriction of foot movement is greater. Therefore, shoes and hockey skates cannot be considered identical. The present study aims at exploring differences amongst bone, skin, and skate marker based motions of the foot during skating. (Abstract shortened by UMI.)

Polynomial regression was used to describe the relationship between lengths of the five muscles of interest and lower extremity joint angle(s). A difference between the genders was observed, so the male and female data were separated and five regression equations (one per muscle) were fitted to each data set. In an attempt to build general regression equations normalization and transformation of the data was performed, but these manipulations of the data did not lead to predictive equations. Addition of leg segment length, for the monoarticular muscles, and height, for the biarticular muscles, as independent variables did significantly increase model fit. The general regression model was quantitatively compared to the leg segment lengths and the actual observed values. It was also qualitatively compared to two other models. Results showed that while the general regression model is good at predicting muscle function, it is not a very accurate predictor of muscle length.

Accumulating biochemical and morphological evidence suggests that apoptosis contributes to neuronal cell death following cerebral ischemia. Recent research which has examined changes in expression of proapoptotic proteins has further strengthened the important role of apoptosis in ischemic cell death. In this thesis I first addressed the role of apoptosis in ischemic death by examining p53, which is itself a complex multifunctional tumor suppresser gene, following transient focal ischemia. Of particular note were the alterations of the anti-apoptosic gene, naip, that were observed under stress conditions. The anatomical distribution of naip expression and neuronal survival following middle cerebral artery occlusion (MCA-o) were closely examined. In experiment I, SHR rats were subjected to 90 minute MCA-o followed by 22.5 hr reperfusion (RP) and compared with sham operated controls. In experiment II, sections obtained from fresh frozen or fixed brain tissue of long-Evans hooded rats (n = 3--4) that had been subjected to hippocampal kindling were used for ISHH or immunohistochemistry for naip expression. Neuronal protection against cerebral ischemia by hippocampal kindling was assessed in experiment III. Hippocampal kindled animals were also used to study the time course of naip expression in the frontoparietal cortex, which is mainly supplied by MCA. Both p53 mRNA and protein were elevated in the ischemic penumbra in experiment I. The induction of p53 peaked within 8--12 hr then returned to basal levels within 24 hr after RP. The short duration of p53 induction in ischemic penumbra may suggest that p53 activate downstream genes responsible for growth arrest, DNA repair or/and apoptosis. Experiment II demonstrated a significant elevation in naip mRNA and proteins in piriform cortex and hippocampus, where neuronal populations known to be protected by kindling. The duration of the elevation lasted up to three weeks. In contrast, naip mRNA and protein remained at baseline levels in regions that are not protected, such as endopiriform cortex and medial thalamus. We also demonstrated that hippocampal kindling attenuated cortical infarct induced by MCA-o to 57.7 +/- 4.6mm3 as compared to 156.5 +/- 12.6mm3 in controls. This neuroprotection was associated with a two to three fold elevation of naip expression in the corresponding areas by kindling treatment. (Abstract shortened by UMI.)

The main objective of this project was to master the electron probe x-ray microanalysis technique to permit one to obtain physiologically meaningful quantitative elemental profiles (Na, Cl, K, P, Mg, Ca & S) for the components of a given cell. The techniques which had to be mastered were: preparation of mammalian (rat) cardiac muscle; 'rapid' cryofixation using a Reichert-Jung MM80E 'impact freezer'; cryosectioning using a Reichert-Jung FC4 cryoultramicrotome; transfer and freeze-drying; electron probe x-rays collection using the EDAX 9100 Series Energy Dispersive X-ray Analysis Systems attached to a Philips TEM 420; quantitative analysis using the Hall equation and thin membrane aminoplastic standards. Different methods of transfer and freeze-drying were compared. Method I-a. Cryotransfer to the electron microscope using a modified Philips Cryotransfer system, freeze-drying in the column of the electron microscope, x-rays collection at low temperature; Method I-b. Cryotransfer to the electron microscope using a modified Philips Cryotransfer system, freeze-drying in the column of the electron microscope, x-rays collection at ambient temperature; Method II. Cryotransfer to a vacuum chamber (Edward-Coating System E306 A) using a precooled metal carrier, freeze-drying in a vacuum chamber while warming at ambient temperature, transfer and x-rays collection at ambient temperature. (Abstract shortened by UMI.)

An ultrastructural study using electron microscopy was undertaken of yolk and yolk sac to elucidate digestive mechanisms and to gather evidence to further substantiate the belief that intracellular digestion of yolk takes place in yolk sac epithelial cells during incubation. Initial work focused on the ultrastructure yolk in unincubated eggs using transmission electron microscopy of thin sections of yolk which had been fixed using conventional and novel fixatives. The next phase of the study involved the ultrastructural comparison of granules from sub-blastodermic fluid from 9 day old embryos, and extracellular yolk attached to the yolk sac of 15 day old embryos with the granules from yolk of unincubated eggs. The third phase of the study was the ultrastructural description of yolk sacs at 3 ages (3 days, 8 days and 15 days of incubation). A transport system for yolk lipid and its digestion products to the embryo was demonstrated ultrastructurally using the Imidazole-buffered Osmium Tetroxide protocol of Angermuller and Fahimi (1982) which enhanced lipid staining. We observed no ultrastructural changes in extracellular yolk granules and matrix particles at any age studied. Granules and matrix particles are taken up by endocytosis, and ultrastructural changes of yolk granules occur in epithelial cells, in acid phosphatase-containing vacuoles (which we have identified as secondary lysosomes), which are part of the functioning intracellular digestive system. We have ultrastructurally demonstrated the transport of lipids, which becomes more evident in 13 day old embryos. On the basis of the above evidence we conclude that yolk is digested in epithelial cells of the yolk sac, and the digestion products enter the blood sinuses and travel in the bloodstream to deliver nutrients to the developing embryo. (Abstract shortened by UMI.)

To study the stimulating effects of retinoic acid on the primary culture of immature rat hepatocyte, we examined the changes in the bile canaliculi formation by observing the cytokeratins 55 kDa and 49 kDa. The formation of the bile canaliculi sheaths was our end point of differentiation. We obtained monolayer hepatocyte culture from 14-day old male Wistar Charles River rats, using the two-step collagenase perfusion method of Seglen (1976), as adapted to preweanling rats by Deschenes et al (1980). All-trans retinoic acid 10$\sp{-5}$M dissolved in 0.1% dimethyl sulfoxide was added to the treated cultures. All cultures were maintained for 48 hours. The organization of cytokeratin was visualized by immunofluorescence using monoclonal antibodies to cytokeratins 55 kDa and 49 kDa. Under the influence of retinoic acid, the number and size of bile canaliculi formed were significantly increased. The bile canaliculi formed and a more complex architecture, such as ramification. Theses observations were confirmed by un-embedded whole mount electron microscopic studies on detergent extracted preparations. In retinoic acid treated colonies, the bile canaliculi appear to be functional as demonstrated by the cellular uptake followed by polarization and secretion of the fluorescein diacetate dye. Gel electrophoresis showed an apparent disparity in the relative quantity of cytokeratin 55 kDa and 49 kDa, especially in the control group. This inequality may be attributed to a selective increase in proteolysis during preparation. It is concluded that the addition of retinoic acid to the media stimulates the differentiation in hepatocyte monolayer cultures. It is possible that retinoic acid induces modification in the hepatocyte gene expression and the formation of bile canaliculi could be associated with changes in the expression of the cytokeratin genes. The two cytokeratins would be coexpressed in response to the treatment with retinoic acid.

In order to understand the role of the dihydropyridine receptor in excitation-contraction coupling in cardiac cells, a thorough study of the structure and function of this molecule is warranted. During the purification of the dihydropyridine receptor on lectin-affinity columns and sucrose density gradients, a high molecular weight protein (360 kDa) was found to co-purify with the receptor. Since several high molecular weight proteins such as ion channels and dystrophin are associated with the cell membrane, the relationship of the 360 kDa protein to these proteins was investigated. The relationship of the 360 kDa protein with other high molecular weight proteins such as dystrophin was investigated using anti-peptide antibodies against dystrophin. The results suggested that the 360 kDa protein was related to $\alpha\sb2$-macroglobulin. In view of the function of $\alpha\sb2$-macroglobulin as a protease inhibitor, it is speculated that the 360 kDa protein may be performing a similar function in heart cells. The rise in Ca$\sp{2+}$ during systole may lead to activation of Ca$\sp{2+}$-sensitive proteases and the presence of a protease inhibitor in these cells may help prevent the proteolytic degradation of essential proteins such as ion channels and dystrophin. Increased proteolytic degradation in Duchenne muscular dystrophy has been shown to be due to high intracellular Ca$\sp{2+}$ levels as a result of sarcolemmal membrane damage. (Abstract shortened by UMI.)

The role of protein kinase C (PKC) in stimulus-secretion coupling in a number of endocrine and exocrine tissues remains poorly understood. In this study, the activation of a specific PKC isozyme during cAMP-mediated secretion from rat parotid acini has been examined. Hydroxylapatite chromatography and immunoblotting studies, with a specific antibody against PKC-$\beta$ utilizing a sensitive enhanced chemiluminescence detection system, indicated that the $\beta$ form was the major PKC isoenzyme in rat parotid gland. Isoproterenol (ISO, 0.1 $\mu$m), a $\beta$-adrenergic agonist, stimulated the translocation of PKC-$\beta$ from the cytosolic to the particulate fraction. A time-course study with this agonist showed that total particulate PKC increased from 50% (resting level) to about 80% during 30 minutes of stimulation, accompanied by a decrease from 50% to 20% in the cytosolic distribution. At low concentrations (up to 0.1 $\mu$M), ISO caused significant redistribution of PKC-$\beta$ during 30 min of stimulation in a dose-dependent manner (Kd = 10 nM). The rate of amylase release evoked by ISO (0.1$\mu$M) was linear during 30 minutes, in good correlation with the translocation of PKC-$\beta$ from cytosol membrane. A permeant cyclic AMP derivative (dibutyryl cAMP) also caused the translocation of PKC-$\beta$ in a dose-dependent manner (Kd $\leq$ 50 $\mu$M). Stimulation with the phorbol ester PMA (10 nM, 100 nM) resulted in both PKC translocation and amylase secretion. Total PKC activity was assayed using a specific peptide substrate and yielded a similar pattern of stimulation of PKC translocation in response to these secretagogues. The accumulated evidence suggests that PKC-$\beta$ becomes activated and translocates during $\beta$-adrenergic-stimulated amylase secretion from rat parotid acini. Therefore PKC-$\beta$ activation may be the common pathway for synthesis stimulus-secretion coupling during stimulation by agonists that cause cAMP synthesis or PIP$\sb2$ hydrolysis.