Prior research has indicated that students of all ages show little understanding of respiration beyond breathing in and out and the need for air to survive. This occurs even after instruction with alternative conceptions persisting into adulthood. Whether this is due to specific educational strategies or to the level of difficulty in understanding a complex system is an important question. The purpose of this study was to obtain a deeper understanding of middle school students' development of mental models of human respiration. The study was composed of two major parts, one concerned with documenting and analyzing how students learn, and one concerned with measuring the effect of teaching strategies. This was carried out through a pre-test, "learning aloud" case studies in which students engaged in one-on-one tutoring interviews with the researcher, and a post-test. Transcript data from the intervention and post-test indicates that all students in this study were successful in constructing mental models of a complex concept, respiration, and in successfully applying these mental models to transfer problems. Differences in the pretest and posttest means were on the order of two standard deviations in size. While findings were uncovered in the use of a variety of strategies, possibly most interesting are the new views of analogies as an instructional strategy. Some analogies appear to be effective in supporting construction of visual/spatial features. Providing multiple, simple analogies that allow the student to construct new models in small steps, using student generated analogies, and using analogies to determine prior knowledge may also increase the effectiveness of analogies. Evidence suggested that students were able to extend the dynamic properties of certain analogies to the dynamics of the target conception and that this, in turn, allowed students to use the new models to explain causal relationships and give new function to models. This suggests that construction of causal, dynamic mental models is supported by the use of analogies containing dynamic and causal relationships.

Lipovitellin, the predominant yolk protein of vertebrate eggs, is a mixture of heat-stable and heat-labile molecules in mature winter flounder eggs. The heat-stable lipovitellin fraction, purified from extracts of unfertilized eggs by brief heat treatment and gel permeation chromatography, contains a single 94 kDa polypeptide. Native lipovitellin also possesses several smaller polypeptides, suggesting that heat-labile lipovitellin contains proteolytic cleavages of the 94 kDa polypeptide which destabilize its structure. The Stokes radii of native, heat-stable and heat-labile lipovitellin are 4.50 nm, 4.26 nm and 5.17 nm, respectively. A polyclonal antiserum raised against heat-stable lipovitellin binds a 175 kDa polypeptide in vitellogenic female winter founder serum, but does not bind any component of male serum. An ELISA constructed from this antiserum identifies serum vitellogenin as a single gel permeation peak with a Stokes radius of 6.70 nm and confirms that vitellogenin is a dimer, while lipovitellin from mature eggs is a monomer. During embryogenesis, lipovitellin is cleaved from a 94 kDa polypeptide to 67 kDa and 26 kDa polypeptides. Proteolytic processing is initially slow, but becomes more rapid between days eight and 12 post fertilization in embryos reared at 4°C–5°C, approaching 50% completion at day ten (tail-bud stage). Processing is essentially complete three days before hatching; nevertheless, major degradation of the lipovitellin polypeptides only occurs in larvae. The Stokes radius of lipovitellin decreases from 4.50 nm in unfertilized eggs to 4.19 nm in late embryos and newly hatched larvae, while processed lipovitellin retains its heat stability relative to other yolk polypeptides. However, 49.2% of the lipid moiety is released from lipovitellin concomitant with cleavage of the 94 kDa polypeptide. Lipovitellin processing may thus render a portion of its stored lipids more accessible to the embryo; alternately, removal of lipid may heighten proteolytic vulnerability of the polypeptide. In either case, only a portion of the lipovitellin particle plays a significant nutritive role for the embryo, while most of the molecule, including its protein component, is reserved for larval use.

Lipids of minced or comminuted muscle foods are particularly susceptible to oxidative deterioration. As a result, antioxidants are added to these products to retard the undesirable changes accompanying oxidation. The efficiency of an added antioxidant is related to its particular location within the product. Thus, directing the added antioxidant to the site where oxidation is initiated and/or propagated is of significant importance. The partitioning of δ-tocopherol between the neutraland the polar lipids of chicken leg muscles was investigated. The two lipid fractions were separated using differential ultracentrifugation techniques. Neutral lipids were obtained after high speed centrifugation of the minced muscle at 130,000 g for 30 min. The polar membrane lipids were collected from a muscle-buffer homogenate (pH 7.5) between 10,000 g for 20 min and 130,000 g for 30 min. The neutral oil collected represented from 11 to 90% of the to triacylglycerols of the minced muscle. The polar membrane lipids represented from 25 to 35% of the total membrane lipids of the muscle. The partitioning of δ-tocopherol between the two lipid fractions depended on the amount of tocopherol added. At low total lipid contents the added δ-tocopherol was present in approximately the same concentration in both muscle lipid fractions. At higher total lipid contents the δ-tocopherol concentration in the membrane lipids increased relative to the neutral lipids. The δ-tocopherol uptake by the lipids of the membranes suspended in buffer increased linearly with tocopherol concentration added in the range of 4 to 4,000 ppm δ-tocopherol on a lipid basis. The membrane lipids contained up to 50% of the added tocopherol. This indicates a high capacity of the membranes for tocopherol incorporation or binding. Studies with model systems consisting of suspended membrane lipids and chicken oil suggested an insignificant exchange of δ-tocopherol between the two lipid fractions when the tocopherol was initially residing in either fraction. This may be due to strong hydrophobic interactions between the antioxidant and the lipids in which it resides. An insignificant uptake of δ-tocopherol by the membrane lipids was also observed when the tocopherol was added in corn oil to a model membrane lipid-chicken oil system. In contrast, when δ-tocopherol was added to the model system dissolved in ethanol the uptake of the membrane lipids increased dramatically. It is proposed that the partitioning of tocopherol between the different lipids of a minced muscle is governed mainly by the relative surface areas of the lipids and the tocopherol concentration in the aqueous phase immediately after its addition. For this purpose the polarity of the tocopherol carrier (solvent) is of particular importance.

Tubuloglomerular feedback (TGF) is a delayed negative feedback mechanism that stabilizes the glomerular filtration rate (renal blood flow) and salt concentration in a single nephron, the basic filtering unit of the kidney. Fluid flow through the nephron exhibits three distinct patterns. It may flow at a constant rate, or it may oscillate in one of two ways: regularly or chaotically. Earlier models indicate that the TGF mechanism plays a role in the mediation of both a constant flow rate and limit cycle oscillations. However, these models do not incorporate the influence of backleak (diffusion) in coupled nephrons (those that are linked anatomically by their vasculature). This dissertation examines the effects of backleak on coupled nephrons. The main result is that backleak stabilizes the system: coupled nephrons with backleak exhibit steady flow rates at higher feedback gains than do those without backleak. This same stabilizing effect was observed in a model of a single nephron with backleak. The model describing the TGF mechanism in two coupled nephrons is also extended in a model of three coupled nephrons. The results suggest that the addition of a nephron to the system may have a destabilizing effect: limit cycle oscillations are exacerbated when a third nephron is added to the system. Numerical methods are developed and implemented to study the predictions given by the bifurcation analysis.

A reduction in the availability of oxidizable metabolic fuels inhibits reproduction. When ovariectomized, steroid-primed hamsters are food deprived for 48 hours, estrous behavior is suppressed. However, the specific neuroendocrine alterations that mediate the suppression or restoration of estrous behavior are unknown. In the following set of experiments, I investigated various possible neuroendocrine alterations associated with nutritional infertility and I found the following. Increasing circulating levels of estradiol can increase lordosis durations in fasted animals, but the suppression of estrous behavior occurs despite increased circulating estradiol levels in ovariectomized, steroid-treated animals. Next, I found that it takes more than 24 h of metabolic inhibitor administration to inhibit lordosis, whereas only 6 h of refeeding is sufficient to restore sexual receptivity. Furthermore, neither plasma insulin nor leptin levels parallel the changes in estrous behavior, suggesting that changes in circulating leptin and insulin probably do not play a critical role in these behavioral changes. Finally, several conditions that inhibit female sexual behavior are thought to be associated with altered corticotropin-releasing hormone (CRH) activity in the brain. Intracerebroventricular (ICV) infusion of CRH or urocortin inhibited estrous behavior in ovariectomized steroid-primed hamsters. Conversely, ICV infusion of the potent CRH receptor antagonist, astressin, prevented the suppression of estrous behavior by food deprivation. Furthermore, astressin blocked the inhibition of estrous behavior by ICV administration of neuropeptide Y and CRH but did not enhance estrous behavior in animals given an inadequate dose of progesterone. Astressin treatment also induced sexual receptivity in nonresponders, animals that do not normally come into heat when treated with hormones. This effect persisted in subsequent weekly tests in the absence of any further astressin treatment. Manipulations that altered sexual behavior did so without affecting food intake and, in most cases, without affecting circulating corticosteroid levels, indicating that the animals were neither ill nor stressed. These results support the hypothesis that endogenous CRH receptor signaling mediates the inhibition of estrous behavior by undernutrition and in other instances of sexual dysfunction suggesting that CRH receptor signaling may be a final common pathway by which a number of distinct conditions inhibit female sexual behavior.

Sexual behavior in female guinea pigs and rats is dependent upon circulating ovarian steroid hormones. The actions of these hormones on behavior are mediated by intracellular receptors located within interconnected brain regions. This complex neural network integrates somatosensory and hormonal information relevant to sexual behavior. An understanding of the anatomy of this network is important for understanding how behavior is generated. This dissertation investigated the neural projections from a region important for the induction of sexual behavior, the ventrolateral hypothalamus. Based on the steroid-sensitive neural network model described in rats, several experiments were designed to test predictions of this neural model in guinea pigs. In the first experiment, estrogen receptor- and estradiol-induced progestin receptor-containing cells were localized in the midbrain, a major projection site of the steroid receptor-rich region within the ventrolateral hypothalamus. In the second experiment, the anterograde tracer Phaseolus vulgaris-Leucoagglutinin, an anterograde tract-tracer, was deposited within the estrogen receptor-containing region of the ventrolateral hypothalamus. Projections from this area were found in most other estrogen receptor-containing sites, including the midbrain central gray, often closely associated with estrogen receptor-containing cells. The third experiment examined the distributions of substance P, a peptide found in ovarian steroid hormone receptor-containing cells in the ventrolateral hypothalamus and estrogen receptor-containing cells in the midbrain central gray. Substance P-immunoreactive boutons were found closely associated with some estrogen receptor-containing cells suggesting substance P modulation of ovarian steroid hormone receptor-containing cells. These connections, taken together with the hypothalamic projections closely associated with estrogen receptor-containing cells in the midbrain, support the idea that some estrogen receptor-containing cells may be directly linked. These studies provide information on the neural connections between estrogen receptor-containing regions and cells which may be important for regulating functions of the steroid hormone sensitive neural network.

Phylogenetic relationships of chimaeroid fishes are investigated in detail. The six genera studied, Callorhinchus, Rhinochimaera, Harriotta, Neoharriotta, Chimaera and Hydrolagus belong to the subclass Chimaeroidei and are the only living representatives of the class Holocephali. The comparative morphology of the lateral line canals, skeleton, tooth plates, secondary sexual characteristics and musculature of all six living genera of chimaeroid fishes is described. Development of the jaws, hyoid arch and ethmoid canal is briefly described for Callorhinchus milii of the family Callorhynchidae. Using anatomical characters a phylogeny of higher level chimaeroid relationships is hypothesized. The infraorder Neochimaeroidi is erected to include Rhinochimaera, Harriotta, Neoharriotta, Chimaera and Hydrolagus on the basis of eight synapomorphies and a new classification of chimaeroid fishes is proposed.

The onset and termination of female rat sexual receptivity are regulated by the activation of steroid hormone receptors. In addition, the onset and termination of sexual receptivity are influenced by mating stimulation. For example, repeated mating stimulation increases sexual behavior in previously unreceptive estradiol-primed female rats. Apparently, sensory cues from the male rat lead to changes in female sexual behavior. The current studies investigated the exact sensory cues responsible for these changes and the mechanisms by which they influence sexual behavior. Mating-induced increases in sexual behavior appear to result largely from vaginal-cervical stimulation (VCS) received from intromissions and ejaculations. Furthermore, it is likely that the effects of VCS are mediated by ligand-independent activation of progestin receptors. Likewise, odors from male rats are necessary for maximal increases in sexual behavior following repeated mating; however, unlike VCS, odors do not seem to influence sexual behavior via a progestin receptor-dependent mechanism. Mating stimulation also accelerates estrous termination. The mechanisms mediating the acceleration of estrous termination following mating were also investigated. It has been hypothesized that mating-induced estrous abbreviation results from down-regulation of progestin receptors; however, several immunocytochemical studies found no evidence supporting this hypothesis. Instead, it appears that the effects of mating stimulation on estrous termination are more complex than previously appreciated. It appears that, while VCS decreases levels of sexual behavior, other sensory cues (e.g. flank stimulation and odors) maintain high levels of sexual receptivity. Thus, the results suggest that estrous duration is the result of a complex interplay between those factors that promote the expression of sexual receptivity and those that inhibit it.

Breastfeeding women experience changes to their bone mineral density over the course of lactation. The exact nature of the relationship between breastfeeding and lactation-induced change in bone density is not well understood but it is known that bone density decreases during lactational amenorrhea and increases after menses resumes. In studies that have explored the relationship between breastfeeding and bone density, variation in breastfeeding behaviors is considered 'noise' to be eliminated. This study explores this relationship by focusing on the role of breastfeeding variation on the rate of bone density change, both before and after menses resumes. To date, most research on breastfeeding and bone density has been conducted by clinical researchers. This study differs from these studies because of an anthropological approach that puts at the forefront of the analysis behavioral variation. Using a biocultural framework, the study design draws from the methods and theories from both biological and cultural anthropology. The theoretical lens, the methodologies, and the theories combine to reveal the complexities in the topic of breastfeeding and bone density. A total of 35 women participated in a six-month longitudinal assessment of bone density change during breastfeeding. They recorded all breastfeeding activity over a 24-hours period each time that their bone mineral density was measured. Results of the study showed that greater intensity of breastfeeding in the amenorrheic months significantly attenuated bone density loss in this population of U.S. women. Amenorrheic women who breastfed with less intensity showed greater decline in their bone mineral density. Similar benefits to the maternal skeleton were not demonstrated in high intensity breastfeeders after menses resumed. Furthermore, the evaluation of the breastfeeding styles of the women in this population showed them to conform to AAP breastfeeding guidelines despite their own assertions that they do not adhere to such recommendations.

The aim of this dissertation was to explore alterations in human skeletal muscle during a controlled period of immobilization and following spinal cord injury (SCI). Study I examined the effects of an imposed period of immobilization of the adductor pollicis (AP) muscle on muscle function and volume in young (18-25 years) and aged (60-75 years) men. Muscle strength and volume of the AP was assessed before and after immobilization. Results from Study I show that although the older and younger adults had disparate losses in muscle volume they experienced similar losses in muscle strength. These results confirm that even short periods of inactivity promote more rapid losses in muscle volume in older adults, while the ability to generate force is maintained. Study II and Study III of this dissertation explored the molecular alterations in human skeletal muscle in response to immobilization or SCI. Muscle biopsies were analyzed at both the transcriptional (microarray analysis, quantitative Real-Time Polymerase Chain Reaction (qRT-PCR)) and translational (Western blotting, Immunohistochemistry (IHC)) level. In Study II, the knee joint of five young men (aged 18-25 years) was immobilized, and muscle biopsies were performed before and after 48h of leg immobilization. Immobilization resulted in increased expression of genes involved in the ubiquitin proteasome pathway and metallothionein function, but no change in respective protein products. However, results of Study II also showed a decrease in gene expression and protein products for the collagens, which are involved in extracellular matrix (ECM) integrity, indicating that disruption to the ECM is an initial step in the muscle atrophy program following immobilization. In Study III, analysis of muscle biopsies taken two and five days post-SCI, compared to healthy controls, showed increased gene expression for genes that encode components of the ubiquitin proteasome pathway, metallothioneins, and secretory leukocyte protease inhibitors. Western blotting and IHC showed that protein products for components of the proteolytic core and the metallothioneins increased by five days post-SCI, and protein products were localized to the ECM. These results indicate that components of the ECM are initial targets of proteolytic activity within the first days following SCI.