Stargazers (Uranoscopidae) have two specialized characters- large volume of bile and a small-size brain. To explain why stargazers need large volume of bile, two hypotheses were proposed: (1) a function of the bile of stargazers is acting as the sex pheromone, and (2) bile enhances calcium uptake efficiency. The brain volume was measured, and the volumes of each part of the brain were also measured. The elementary investigations indicate that the stargazers have larger bile volume ratio and smaller brain weight ratio than other fishes reported in the present studies. The bile volumes are no significant difference between the female stargazers and the male stargazers, the bile volumes showed no monthly difference. Besides, the number of olfactory epithelium and the neuron density of the telencephalon in stargazers were not more than other fishes, the function of sex pheromone of bile can not be confirmed. The cranium hardness, bone density, and calcium content in stargazers are significantly more than other fishes. Most fish uptake calcium by the gill and the intestine from seawater or food. However, stargazers often hide in the sand and wait for the prey for most of the time, less water flow through the gills are expected. Therefore stargazers possibly uptake calcium through the intestine. Efficiency of the bile to aid calcium uptake has to be examined by experiments. The paraffin histology has been taken in various parts of the brain. Crista cerebelli is the center for sensing mechanical vibration; the volume of stargazer¡¦s crista cerebelli is higher than other fishes. Stargazers have large saccular otolith compare to the whole brain. Studies on the lateral line and acoustic sense of stargazers are new research topics. Furthermore, decrease in brain size in stargazers is for the purpose of reducing the oxygen consumption, so as to hiding in the sand. Stargazers are one of the fisheries species on western Taiwan coast. However there are very few studies on the stargazers in Taiwan; we should understand more about them in order to protect and consume the stargazers in a better way.

Skeletal muscle fatigue can be defined as the inability to produce a desired amount of force. Fatigue can not only limit athletic performance and rehabilitation, but it can affect one's ability to perform every day activity as well. Despite extensive investigation of muscle fatigue, little is known about the exact mechanisms that result in decreased muscle performance. It likely involves several factors that are themselves dependent upon activation patterns and intensity. The process of excitation-contraction (EC) coupling is of particular importance with respect to regulation of force production. The release of calcium (Ca²⁺) from the sarcoplasmic reticulum (SR), which is stimulated by the depolarization of the sarcolemma, causes muscle contraction. The SR Ca²⁺-adenosine triphosphatase (ATPase) drives the translocation of two Ca²⁺ ions into the SR, utilizing the energy derived from the hydrolysis of one adenosine triphosphate (ATP) molecule. The process of SR Ca²⁺ uptake causes muscle relaxation. It has been proposed that both glycogen and glycolytic enzymes are associated with the SR membrane (SR-glycogenolytic complex). Interestingly, glycogen phosphorylase, an enzyme involved in glycogen breakdown, seems to be associated with the SR-glycogenolytic complex through its binding to glycogen. The presence of the SR-glycogenolytic system may serve to locally regenerate ATP utilized by the SR Ca²⁺-ATPase. The purpose of the present study was to investigate the effects of prolonged muscle contraction on glycogen concentration, glycogen phosphorylase content and activity, and maximum Ca²⁺ uptake rate associated with the SR. Tetanic contractions, elicited once per second for 15 minutes, significantly reduced glycogen associated with SR to 5.1% of control from 401.17 ± 79.81 to 20.46 ± 2.16 mg/mg SR protein (£ 0.05). The optical density of glycogen phosphorylase from SDS-PAGE was significantly reduced to 21.2% of control (£ 0.05). Activity of glycogen phosphorylase, in the direction of glycogen breakdown, was significantly reduced to 4.1% of control (£ 0.05). Pyridoxal 5'-phosphate (PLP) concentration, a quantitative indicator of glycogen phosphorylase content, was significantly reduced to 3.3% of control (£ 0.05). Maximum SR Ca²⁺ uptake rates were significantly reduced to 80.8% of control (£ 0.05). These data suggest reduced glycogen and glycogen phosphorylase may be involved, either directly or indirectly, in a mechanism that causes decreased SR Ca²⁺ uptake normally found in fatigue. / Master of Science

Sugar (primarily sucrose) has been a part of the daily diet for literally hundreds of years, but research is now suggesting that sugar intake can be detrimental to our health. In particular, excessive consumption of simple sugars with high glycemic index (GI) values have been shown to cause overeating and weight gain. As well, elevated postprandial hyperglycemia can result after consuming sugars and this has been linked to disease formation and progression, the development of advanced glycation endproducts, inflammation and increased mortality rates. Honey has been recognised as having a number of beneficial health properties, including slower uptake into the bloodstream, a pharmacological action of reducing blood glucose levels and a high level of bioavailable antioxidants, all of which may mean that honey could be less harmful to health than sucrose in the diet. This study was therefore designed to investigate the health benefits of honey in the diet as a replacement for sucrose, using small animal studies. As well, because of the interest in using honey as a replacement for sucrose in sweetened dairy foods, a small number of in vitro investigations were carried out to determine whether honey could retain its bioactive properties when combined with milk/dairy products. Using the in vitro studies, it was shown that the combination of milk with honey had no effect on either the antibacterial or antioxidant capabilities of honey. During the animal feeding studies a number of significant findings were observed. In the earlier work it was shown that honey had a significant effect on protein metabolism when fed for 14 days at a level of 600 g/kg diet (comprising 480 g sugars and 120 g water) compared with animals fed an equivalent amount of sucrose. In this study, honey-fed rats exhibited significantly lower weight gains (p less than 0.001), food intake (p less than 0.05) and nitrogen intakes (p less than 0.05) and significantly higher faecal nitrogen outputs (p less than 0.05) compared with sucrose-fed rats. Animals fed a diet consisting of 480 g/kg of mixed sugars as in honey generally exhibited protein metabolism parameters that were comparable to those of the sucrose-fed rats, suggesting that the effects of honey on protein metabolism were not due solely to its distinctive sugar composition. Furthermore, in another study that specifically investigated the effects of honey on weight regulation, honey (100 g/kg diet) resulted in significantly reduced weight gain after 6 weeks (p less than 0.01) compared with animals fed the same amount of sugars as sucrose, although food intake was not reduced in this study. Percentage weight gains were shown to be comparable between honey-fed rats and those fed a sugar-free diet, suggesting that differences in glycemic control may be partly responsible for the results seen. Fasting lipid profiles and blood glucose levels were also measured in this study, but no significant differences were observed between diet groups. During long-term (12 months) feeding weight gain was again significantly reduced in rats fed honey (p less than 0.05) and a sugar-free diet (p less than 0.01) compared with those fed sucrose, the weights of honey-fed rats and those fed the sugar-free diet being comparable at the end of the study. In addition, blood glucose levels were significantly lower (p less than 0.001), and HDL-cholesterol levels significantly higher (p less than 0.05) in animals fed honey compared with those fed sucrose after 52 weeks, but no differences in these parameters were observed between rats fed sucrose and a sugar-free diet. No other significant differences in lipid profiles were observed. Immunity measures were improved after feeding honey or sucrose for 52 weeks, animals in both of these diet groups having significantly higher levels of neutrophil phagocytosis compared with those fed the sugar-free diet (both p less than 0.0001). In addition, the percentage of leukocytes that were lymphocytes was significantly higher in honey-fed rats at the end of the study. Furthermore, levels of oxidative damage in aortic collagen were significantly reduced in rats fed honey or the sugar-free diet (both p less than 0.05) compared with those fed sucrose after 52 weeks. Full body DEXA scans were also undertaken in this 12-month study to assess body fat levels and bone mineral composition and density, although they revealed few statistically significant differences. Percentage body fat levels were shown to be nearly 10% lower in honey-fed rats compared with sucrose-fed animals at the end of the study (p less than 0.05), but no other significant differences between diet groups were observed. With one exception, no differences in bone mineral composition or bone mineral density were observed between the three diet groups after 52 weeks. This data agreed with the results generated from two earlier studies that showed that feeding honey short-term (for 6-8 weeks) to rats that were either calcium-deficient or fed a low calcium diet had no effect on bone calcium levels, bone mineral content, bone mineral density or bone breaking parameters. Lastly, long-term feeding of honey to rats had a number of statistically significant effects on anxiety and cognitive performance when assessed using animal maze tasks. Anxiety-like behaviour was significantly reduced in honey-fed rats overall compared with those fed sucrose (p = 0.056) or a sugar free diet (p less than 0.05). Spatial memory was also better in honey fed-rats throughout the 12 month study, these animals not displaying the same degree of age-related spatial memory loss seen in the other two diet groups. No significant differences in recognition memory or learning capability were observed between diet groups after 52 weeks. In conclusion, both short-term and long-term feeding of honey result in a number of health benefits compared with eating similar amounts of sucrose. These include less weight gain, improved immunity, reduced levels of oxidative damage and improved cognitive performance.. These effects of honey are likely to occur through a number of different processes, although the presence of high concentrations of antioxidants and other minor components in honey are likely to be important contributors. Honey may therefore help to improve human heath if it is used as an alternative to sucrose in foods and beverages, although feeding studies in humans are required to assess its efficacy. In addition, more animal studies are needed to assess which features of honey (e.g. fructose content, antioxidant content and bioactivities) are required to achieve optimal effects, and to determine what impact heating and food processing may have on the beneficial health effects of honey.

Mitochondria are dynamic organelles known primarily for their roles in oxidative metabolism and programmed cell death. Both of these processes are regulated by the mitochondrial matrix calcium concentration. Little is known about how mitochondrial calcium is regulated: no plant mitochondrial Ca2+-ATPase pumps or no mitochondrial Ca2+ channels have been identified to date. In addition, little is known concerning any physical interactions between mitochondria and endoplasmic reticulum (ER), an important cellular calcium store, and how these modulate cellular calcium fluxes. In this work stable transgenic Arabidopsis lines expressing fluorescent marker proteins were generated to allow visualisation of mitochondria and the ER in the same cells, and to measure mitochondrial calcium fluxes using aequorin. According to my results, there is a physical association between mitochondria and ER and this association cannot be disrupted by chemical treatments (latrunculin B, methyl viologen and antimycin A). As part of this work I identified an Arabidopsis gene, Mitochondrial Calcium Uptake 1 (MCU1), which encodes a protein with features that suggest a role in mitochondrial calcium dynamics. Fluorescent protein fusions of this protein demonstrated that it localizes to mitochondria. An Arabidopsis T-DNA line was identified with an insertion in MCU1. However, little effect of the insertion on transcript abundance of MCU1 was observed.

Previous research regarding aquatic acidification has examined the protonation of the carbonate and does not consider calcium to be a limiting factor. This is the first study to suggest that pH may affect the uptake of calcium in crustacean gills. This project describes ion transport mechanisms present in the cell membranes of white river shrimp Litopenaeus setiferus gill epithelium, and the effects of pH on the uptake of calcium by these means. Partially purified membrane vesicles (PPMV) of shrimp gills were prepared through a homogenization process that has been used previously to define ion transport in crab and lobster gill tissues. In the current study, shrimp gill PPMV calcium uptake at 50 µM, and 250 µM was greatest at pH 7.0 (p=0.01, p=0.0001). A valinomycin/K+ induced membrane potential (PD) at pH 7.0 significantly increased (p=0.003) calcium uptake from that observed in the absence of a PD. An induced PD at pH 8.0 significantly increased (p=0.003) calcium uptake from that observed in the absence of a PD, however, was not significantly greater than uptake at pH 7.0 in the presence of a PD (p=0.05). Amiloride (2mM) treatments, and amiloride (2mM) + verapamil (100µM) cocktail treatments showed significant decrease in calcium uptake from the control (p=0.03), however, they were not different from each other. This indicates an electrogenic carrier with two driving forces: calcium concentration, and asymmetric exchange stoichiometry.

25-Hydroxyvitamin D3[25(OH)D3] is a metabolite of vitamin D3 that has long been considered to be an inactive precursor of the hormonally active metabolite 1,25- dihydroxyvitamin D3[l,25(OH)2D3]; consequently very few studies have addressed the potential biological activity of 25(OH)2D3. However, it is known that 100 nM 25(OH)2D3 increases calcium transport in the perfused duodenal loop of the chicken to 200% of controls within 20 minutes. The hypothesis of the current study is that 25(OH)2D3 may be a hormonally active metabolite and its effects can be studied in isolated chick enterocytes. To begin testing this postulate, time course studies of 45Ca uptake were undertaken in isolated intestinal cells (from 7 wk chicks). After establishing the basal uptake of 45Ca for 5 minutes, cells were treated with vehicle(< 0.01% v/v ethanol, final concentration) or 25 nM, 50 nM, 100 nM, or 300 nM 25(OH)2D3 and samples were taken at T = 1, 3, 5, 7, and 10 min. With increasing concentrations of steroid, the enterocyte 45Ca decreased. The optimal concentration of 100 nM 25(OH)2D3 induced the most rapid response: within 1 min 45Ca decreased to 54% of controls (P < 0.001) and 70% of the controls at T= 3, 5, and 7 min (P < 0.01 to < 0.05, relative to controls). Comparison of the 7- min time points for 25 nM, 50 nM, 100 nM, and 300 nM 25(OH)2D3 appeared to yield a biphasic dose response curve with values of 45Ca observed at 99% (NS, not significant), 75% (P < 0.05), 70%(P < 0.01%), and 80% (NS) of corresponding controls, respectively. Physiological levels of 24,25(OH)2D3 (6.5 nM) inhibited the action of 100 nM 25(OH)2D3 in isolated chick enterocytes. Time course studies with isolated enterocytes from 14 wk and 28 wk chickens treated with 100 nM 25(OH)2D3 also showed decreased responsiveness: at T= 1 min 45Ca levels in 7 wk, 14 wk, and 28 wk were 54% (P < 0.01), 83% (NS), and 80% (NS) of corresponding controls, respectively. Experiments with the calcium channel activator BAY K8644 (2 μM) and protein kinase A (PKA) activator forskolin (20 μM) revealed enhanced levels of 45Ca at T= 10 min that were 132% and 140% of corresponding controls, respectively (each, P < 0.05). Phorbol ester treatment of the cells resulted in significant increases in the levels of 45Ca between the treated cells and corresponding controls at T=7 and 10 min. Cells treated with 100 nM 25(OH)2D3 revealed 89.8% and 78.4% increases above controls in PKA activity at T =1 min (P < 0.05) and T=3 min, relative to corresponding controls. However, there was no evidence for the activation of PKC by 25(OH)2D3 during the time period studied.

No description available.