Medical educators should hold limited expectations of the SDLRS to measure medical students' readiness to engage in self-directed learning. The definitions and theoretical assumptions that inform readiness for self-directed learning should be reconsidered. Alternative approaches to studying self-directed learning should be explored.
Abstract. Several studies have indicated that arginine vasotocin (AVT), a nonapeptide closely related to vasopressin (ADH) and oxytocin (OT), may act as a pineal antigonadotrophic factor. The present studies were designed to investigate the effects of AVT on the luteinizing hormone (LH) and prolactin (Prl) release induced by sequential steroid priming of ovariectomized (OVX). rats. Sprague-Dawley rats were used 6–8 weeks post-OVX. After implantation of an intra-atrial bleeding catheter, animals were primed with 5 μg of oestradiol benzoate (EB) at 08.00 h on the next morning. Forty-eight hours later 1.5 mg of progesterone (P) was injected and animals were divided into groups which received either saline, AVT (1 of 4 doses), ADH, or OT. The saline or peptides were infused via the intra-atrial catheter at 10.00, 11.00, 12.00, and 13.00 h. Hourly blood sampling was performed at 11.00–18.00 h, and at 21.00 h. The 11.00, 12.00, and 13.00 h samples were taken 10 min after saline or peptide infusion. LH and Prl responses to the peptide infusions could be divided into pre-surge and surge effects. AVT caused a slight, but significant elevation of the normally low levels of LH and Prl which occurred before the onset of their surges. Only the highest dose of AVT (1.0 μg) blocked the LH surge. ADH, however, was capable of stimulating LH and Prl release during the pre-surge period and of inhibiting the LH surge. AVT at a dose of 0.5 or 1.0 μg specifically blocked the onset of the Prl surge, causing Prl to drop to its lowest level at 14.00 h - the time at which Prl levels were maximal in saline-treated animals. After this initial inhibition, however, Prl levels rebounded to show a delayed surge. OT infusion, on the other hand, caused a significant augmentation of the Prl surge. These data indicate that AVT may specifically block the onset of the Prl surge seen after sequential steroid priming of OVX rats, while OT may facilitate the Prl surge.
The pineal complex of rodents is made up of a pineal gland which developmentally always originates from the area between the habenular and posterior commissure and a pineal sac which is continuous with the choroid plexus of the third ventricle. At the light-microscopic level, this sac appears to be identical to the choroid plexus.The pineal sac abuts the deep and superficial pineal glands of the golden hamster. In the PET mouse, gerbil, kangaroo rat, and Chinese hamster, the sac is contiguous with only small areas of the pineal gland. This sac never abuts true pineal parenchyma in the albino rat. The variability of the relationship between this sac and pineal parenchyma indicates that the sac may not be the main physiological route of pineal secretion. Venous drainage of the pineal gland consistently seemed to be into the superior sagittal sinus by means of the vena cerebri magna.
The pineal gland of the 13-lined ground squirrel (Citellus tridecemlineatus) has been examined at the light and electron microscopic level. This gland is composed of low-density parenchymal cells interspersed among which are occasional glial, vascular and neural elements. Punctuating the glandular parenchymal mass are prominent perivascular and intercellular spaces. The parenchymal cells possess numerous mitochondria and less prominent profiles of rough and smooth-surfaced endoplasmic reticulum. Golgi apparatus, microtubules and lipid droplets of varying size and electron density constitute regular cytoplasmic features, with dense-core vesicles being present occasionally. The parenchymal cells have numberous processes. One among these in each cell extends for several micra to terminate in a bulbous expansion containing both clear and dense-core vesicles and occasional electron-dense inclusions. These bulbous terminals are found within the perivascular and intercellular spaces where they course in close proximity to both other parenchymal elements and axon terminals. Glial cells and their processes invest the pineal periphery and incompletely separate the parenchymal cells.
The ultrastructure of rat masseter muscle was examined at 15 min, 1 and 6 h, and 1 and 2 days following a single injection of 2% lidocaine. Lesions developed within 15 min. The plasma membrane was disrupted and invaginated. The nuclei were pyknotic and the mitochondria appeared swollen. The myofibrils separated and became disoriented. By 1 and 6 h, these changes were severe. By 1 day, the macrophages appeared in damaged myofibers. The presence of a few presumptive myoblasts signaled the onset of regeneration. By 2 days, presumptive myoblasts formed within the basement membrane. The basal lamina proved most resistant to injury. Regeneration of masseter muscle following the damage produced by lidocaine appeared discontinuous in nature. The singly nucleated presumptive myoblasts seemed to arise within the lesions.
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