by Lai Wing Hong Kevin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 63-74). / Acknowledgments --- p.i / Abbreviations --- p.ii / Abstract --- p.1 / Chapter Chapter 1 --- General Introduction --- p.3 / Chapter 1.1 --- Advantages of Antisense Oligonucleotides Inhibition --- p.4 / Chapter 1.2 --- The Uses of Antisense Oligonucleotide in Leukemic Therapy --- p.5 / Chapter 1.3 --- Oncogenes in the Pathogenesis of Leukemia --- p.6 / Chapter 1.4 --- Apoptosis and Apoptosis-Related Genes --- p.9 / Chapter 1.5 --- Protooncogene bcl-2 --- p.10 / Chapter 1.6 --- Bcl-2 Homologues --- p.11 / Chapter 1.7 --- Regulation of Apoptosis by Other Genes --- p.13 / Chapter 1.8 --- Promyelocytic Leukemia HL-60 Cell Line --- p.15 / Chapter 1.9 --- Aim of Project --- p.16 / Chapter Chapter 2 --- Chemical Synthesis of DNA Oligonucleotides / Chapter 2.1 --- Introduction --- p.17 / Chapter 2.2 --- Materials and Methods --- p.20 / Chapter 2.3 --- Results --- p.24 / Chapter 2.4 --- Discussion --- p.26 / Chapter Chapter 3 --- The Apoptotic Effects of TPA and Ouabain on the Promyelocytic Leukemic HL-60 cell line / Chapter 3.1 --- Introduction --- p.30 / Chapter 3.2 --- Materials and methods --- p.33 / Chapter 3.3 --- Results --- p.40 / Chapter 3.4 --- Discussion --- p.44 / Chapter Chapter 4 --- Effect of Antisense Oligonucleotides on TPA-Induced Apoptosisin Leukemic HL-60 cells / Chapter 4.1 --- Introduction --- p.48 / Chapter 4.2 --- Materials and Methods --- p.49 / Chapter 4.3 --- Results --- p.52 / Chapter 4.4 --- Discussion --- p.54 / Chapter Chapter 5 --- General Discussion --- p.57 / References --- p.63

Tsang, Chi Keung. / "November 2011." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 103-116). / Abstracts in English and Chinese. / Abstract --- p.I / 摘要 --- p.III / Acknowledgement --- p.IV / Table of content --- p.V / List of Figures --- p.VIII / List of Tables --- p.XI / Abbreviations --- p.XII / Chapter Chapter 1: --- INTRODUCTION --- p.1 / Chapter 1.1. --- Hepatocellular carcinoma --- p.2 / Chapter 1.1.1. --- Etiological factors --- p.11 / Chapter 1.1.1.1. --- Chronic Hepatitis and Liver Cirrhosis --- p.13 / Chapter 1.1.1.2. --- HBV --- p.13 / Chapter 1.1.1.3. --- HCV --- p.17 / Chapter 1.1.1.4. --- Male gender --- p.20 / Chapter 1.1.1.5. --- Aflatoxin B1 exposure --- p.21 / Chapter 1.2. --- Genomic abnormalities in HCC --- p.23 / Chapter 1.3. --- GEF-H1 --- p.24 / Chapter 1.4. --- RhoA --- p.26 / Chapter 1.5. --- Epithelial-Mesenchymal Transition (EMT) --- p.29 / Chapter 1.6. --- Aims of Thesis --- p.31 / Chapter Chapter 2: --- MATERIALS AND METHODS --- p.32 / Chapter 2.1. --- Materials --- p.33 / Chapter 2.1.1. --- Chemicals and Reagents --- p.33 / Chapter 2.1.2. --- Buffers --- p.35 / Chapter 2.1.3. --- Cell Culture --- p.37 / Chapter 2.1.4. --- Nucleic Acids --- p.38 / Chapter 2.1.5. --- Enzymes --- p.39 / Chapter 2.1.6. --- Equipments --- p.40 / Chapter 2.1.7. --- Kits --- p.41 / Chapter 2.1.8. --- Antibodies --- p.42 / Chapter 2.1.9. --- Software and Web Resources --- p.43 / Chapter 2.2. --- Fluorescence In Situ Hybridization (FISH) --- p.44 / Chapter 2.2.1. --- Probe Preparation --- p.44 / Chapter 2.2.1.1. --- Human Bacterial Artificial Chromosome (BAC) probe preparation --- p.44 / Chapter 2.2.1.2. --- Nick translation --- p.44 / Chapter 2.2.2. --- Hybridization --- p.45 / Chapter 2.3. --- Genomic DNA extraction --- p.47 / Chapter 2.4. --- Copy number analysis --- p.48 / Chapter 2.5. --- Exon Sequencing analysis --- p.49 / Chapter 2.5.1. --- PCR amplification of GEF-H1 exons --- p.49 / Chapter 2.5.2. --- Cycle sequencing --- p.49 / Chapter 2.6. --- Ectopic expression of GEF-H1 in immortalized hepatocyte cell line --- p.52 / Chapter 2.6.1. --- Construction of GEF-H1 expressing vector --- p.52 / Chapter 2.6.2. --- Sub-cloning --- p.52 / Chapter 2.6.3. --- Transfection and clonal selection --- p.53 / Chapter 2.7. --- Gene Expression Analysis by Quantitative RT-PCR --- p.55 / Chapter 2.7.1. --- Total RNA extraction --- p.55 / Chapter 2.7.2. --- qRT-PCR analysis for gene expression --- p.55 / Chapter 2.8. --- Western blot --- p.58 / Chapter 2.9. --- Functional Analysis --- p.60 / Chapter 2.9.1. --- Cell viability (MTT) assay --- p.60 / Chapter 2.9.2. --- Cell proliferation assays (BrdU-incorporation) --- p.60 / Chapter 2.9.3. --- Mitomycin C treatment --- p.61 / Chapter 2.9.4. --- Migration and Invasion assays --- p.63 / Chapter 2.9.5. --- Wound healing assay --- p.65 / Chapter 2.9.6. --- Transient knock-down of RhoA --- p.65 / Chapter 2. --- 10. Immuno-fluorescent imaging --- p.66 / Chapter 2. --- 11. In vivo tumorigenic study of GEF-H1 by subcutaneous injection --- p.68 / Chapter 2. --- 12. Statistical analysis --- p.69 / Chapter Chapter 3: --- RESULTS --- p.70 / Chapter 3.1. --- Verifying copy number gain of GEF-H1 in high GEF-H1 expressing HCC --- p.71 / Chapter 3.2. --- Verifying if there is any GEF-H1 exon point mutation in HCC --- p.75 / Chapter 3.3. --- Functional roles of GEF-H1 in HCC --- p.77 / Chapter 3.4. --- GEF-Hl-induced functions were RhoA independent --- p.83 / Chapter 3.5. --- GEF-H1 Induction of Epithelial-mesenchymal transition in HCC --- p.88 / Chapter 3.6. --- GEF-H1 induced tumorigenicity of MIHA cells --- p.95 / Chapter Chapter 4: --- DISCUSSIONS --- p.96 / Chapter 4.1. --- GEF-H1 in HCC and other cancers --- p.97 / Chapter 4.2. --- GEF-H1 promotes cell motility --- p.98 / Chapter 4.3. --- GEF-H1 induced tumorigenicity --- p.100 / Chapter Chapter 5: --- CONCLUSIONS AND PROPOSED FUTURE INVESTIGATIONS --- p.101 / Chapter Chapter 6: --- REFERENCES --- p.103

Uveal Melanoma (UM) is the most common malignant intra-ocular tumor in adults. Forty-five percent of UM patients develop metastasis within fifteen years of the initial diagnosis. Cutaneous Melanoma (CM) is a highly metastatic cancer that accounts for the majority of skin cancer deaths. Current treatments are not especially effective for the metastatic phase of the disease. Therefore, the identification of new molecular targets that can be exploited in the clinic are needed. / KISS1 is a putative human metastasis suppressor gene. The purpose of this study was to investigate the expression of KISS1 in melanoma and its potential value as a prognostic marker. / From results in vitro and in vivo we were able to characterize KISS1 in UM for the first time as well as its expression at the protein level, in CM. The correlation between KISS1 expression and UM survival rate suggests an important role for KISS1 as a prognostic marker in this tumor.

[Truncated abstract] The placenta forms a barrier regulating the transfer of gases, nutrients and wastes between the mother and the developing conceptus, and also produces hormones affecting both the fetus and the mother. This barrier is formed by the differentiation of the outer layer of the blastocyst- the trophoblast- to facilitate implantation and subsequent invasion of the uterus. The trophoblast consists of an underlying proliferative pool of cytotrophoblasts, which differentiate to replenish the overlying continuous, multi-nucleated syncytiotrophoblast that forms the barrier between the mother and fetus. Moreover, the location of the syncytiotrophoblast directly in contact with the maternal circulation suggests an endothelial role for the trophoblast regulating blood flow, thrombosis and immune cell adhesion. Disruption to the function of the human trophoblast may result in preeclampsia, a maternally manifested disorder of pregnancy characterised by hypertension and proteinurea. Blood flow to preeclamptic placentae is reduced and the cytotrophoblast pool is diminished; however the exact cause (or causes) remains elusive. Many potential causes are hypothesised, including endothelial damage, premature remodelling of maternal spiral arteries, increased oxidative stress and impaired trophoblast differentiation and apoptosis. Caspase-14 is an unusual caspase in that it is not involved in apoptosis. Furthermore, it possesses a limited, predominantly epithelial, tissue distribution. In the epidermis, caspase-14 is expressed in the apical differentiating layers. Here it cleaves profilaggrin to stabilise intracellular keratin intermediate filaments, and indirectly provides natural hydration and UV protection to the corneocytes. Thus, caspase-14 is vital to the maintenance of the barrier function of the skin. ... As differentiation-associated genes were elevated in the absence of caspase-14, this implies that caspase-14 suppresses biochemical trophoblast differentiation. The cytoskeletal keratin network was also examined following RNA Interference. The synthesis of cytokeratin 18 was significantly enhanced after caspase-14 suppression during BeWo differentiation, linking caspase-14 with keratin homeostasis. Therefore caspase-14 suppresses trophoblast differentiation, potentially through modulation of the cytoskeletal keratin filament network. The precise mechanism remains to be elucidated, however the identification of pathways regulated by caspase-14 advances our knowledge of trophoblast differentiation and potential causes of disorders of pregnancy. In summary, caspase-14 appears to be involved in the suppression of differentiation in the human trophoblast. As disorders of pregnancy such as preeclampsia often feature disturbed differentiation and a diminished cytotrophoblast pool, a greater understanding of caspase-14 biology in the human placenta could lead potential therapies for various disorders of pregnancy.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

No description available.

No description available.

This thesis aimed to, first, examine the effects of the addition of whey protein or casein protein to common carbohydrate-electrolyte (CE) solutions on post-exercise rehydration; second, examine the effects of various contents of whey protein in CE solutions on post-exercise rehydration; and third, investigate the mechanisms on the increased fluid retention after the ingestion of CE plus whey protein solutions. / The first study (Chapter 4) of this thesis examined the effects of CE solution added with a certain amount of whey or casein protein on post-exercise rehydration. Ten young healthy males (mean ± SEM, age: 20.7 ± 0.4 years; body weight (BW): 65.4 ± 2.0 kg; maximal oxygen uptake (VO₂ₘₐₓ): 60.7 ± 1.9 mL·kg⁻¹·min⁻¹) were recruited in this study. Three main experimental trials were conducted in a randomized single-blinded crossover design and separated by at least 7 days between any two of them. In each main trial, subjects ran for 60 min at 65% VO₂ₘₐₓ on a treadmill in a warm and humid environment (24 °C, 60% relative humidity (RH)), which was followed by a 4-hour recovery period. During recovery, the subjects were provided with either a common CE solution, or a CE with whey protein (CW) solution, or a CE with casein protein (CC) solution. The three solutions were matched for energy and electrolyte content and were provided in six equivalent volumes at 30 min intervals with a total volume equivalent to 150% of their BW loss. The nude BW, urine samples, and capillary blood samples were collected before and after exercise and at the end of each hour during recovery. After exercise, the subjects lost approximately 2.3% of their pre-exercise BW in all trials. Total urine volume after recovery was higher in the CE and CC trials than in the CW trial (CE vs. CW vs. CC: 1184 ± 120 mL vs. 1005 ± 68 mL vs. 1256 ± 130 mL, p < 0.05), which induced greater fluid retention in CW trial compared with both CE and CC trials (CE vs. CW vs. CC: 46.9 ± 5.2% vs. 54.9 ± 2.9% vs. 45.8 ± 5.5%, p < 0.05). By the end of recovery, the urine specific gravity (USG) was lower in the CE trial than in both CW and CC trials (CE vs. CW vs. CC: 1.002 ± 0.001 g·mL⁻¹ vs. 1.004 ± 0.001 g·mL⁻¹ vs. 1.004 ± 0.000 g·mL⁻¹, p < 0.05). In addition, the urine osmolality was lower in the CE trial than in both CW and CC trials after recovery (CE vs. CW vs. CC: 111 ± 18 mmol·kg⁻¹ vs. 181 ± 14 mmol·kg⁻¹ vs. 195 ± 23 mmol·kg⁻¹, p < 0.05). However, no difference was found in the changes of plasma volume among trials throughout recovery. These results suggested that during a 4-hour recovery after 60 min run which induced about 2% BW loss, the CE plus whey protein solution was more effective in fluid retention compared with the isocaloric CE or CE plus casein protein solution. / The second study (Chapter 5) was conducted to examine the effects of various contents of whey protein in CE solutions on post-exercise rehydration; meanwhile, the mechanisms on the greater fluid retention after the ingestion of CE plus whey protein solutions were investigated as well. Ten young healthy males (mean ± SEM, age: 22.0 ± 0.7 years; BW: 64.5 ± 1.9 kg; VO₂ₘₐₓ: 59.8 ± 1.9 mL·kg⁻¹·min⁻¹) finished five main experimental trials in a randomized single-blinded crossover manner and separated by at least 7 days. After a 60-min run at 65% VO₂ₘₐₓ on a treadmill in each main trial, a 4-hour recovery period was carried out. During recovery, five solutions of 1) a CE solution with high CHO content (CE-H); 2) a CE solution with low CHO content (CE-L); 3) a CE solution with high content of whey protein (CW-H); 4) a CE solution with medium content of whey protein (CW-M); and 5) a CE solution with low content of whey protein (CW-L) were consumed by the subjects randomly. The electrolyte content was matched, whereas CE-H, CW-H, CW-M, and CW-L solutions were matched for energy density, CE-L and CW-H solutions were matched for CHO content. The total volume consumed by subjects was 150% of the BW loss, and the solutions were provided in six equal volumes at 30 min intervals during recovery. The nude BW, urine samples, and capillary and venous blood samples were obtained before and after exercise and at the end of each hour during recovery. The results showed that the subjects lost about 2.2% of BW after exercise. By the end of the recovery, the total urine volume was smaller in the CW-M trial than in the CE-H trial (CE-H vs. CW-M: 1295 ± 103 mL vs. 1049 ± 130 mL, p < 0.05), whereas the CW-H trial was smaller than the CE-H, CE-L, and CW-L trials (CE-H vs. CE-L vs. CW-L vs. CW-H: 1295 ± 1033 mL vs. 1284 ± 90 mL vs. 1141 ± 58 mL vs. 891 ± 73 mL, p < 0.01). The less urine production in the CW-M and CW-H trials resulted in a greater fluid retention compared with CE-H, CE-L, and CW-L trials (CE-H vs. CE-L vs. CW-L vs. CW-M vs. CW-H: 38.4 ± 5.2% vs. 36.1 ± 4.3% vs. 43.0 ± 3.8% vs. 51.0 ± 5.7% vs. 55.4 ± 3.8%, p < 0.05). The CE-H and CE-L trials showed lower USG and urine osmolality compared with the CW-L, CW-M, and CW-H trials at the end of recovery (p < 0.05). In addition, the plasma osmolality of the CE-L trial was lower than that of the CW-L, CW-M, and CW-H trials at the 1st hour of recovery (CE-L vs. CW-L vs. CW-M vs. CW-H: 274 ± 4 mmol·kg⁻¹ vs. 291 ± 4 mmol·kg⁻¹ vs. 301 ± 6 mmol·kg⁻¹ vs. 293 ± 6 mmol·kg⁻¹, p < 0.05). The plasma volume was lower in the CE-L trial than that in the CW-H trial at the 2nd and 3rd hour, and the CE-L trial reached the lowest plasma volume than the other four trials by the end of recovery (p < 0.05). The aldosterone concentration was lower in both CE-H and CE-L trials compared with the CW-M and CW-H trials after recovery (CE-H vs. CE-L vs. CW-M vs. CW-H: 228 ± 100 pg·mL⁻¹ vs. 211 ± 51 pg·mL⁻¹ vs. 336 ± 85 pg·mL⁻¹ vs. 333 ± 70 pg·mL⁻¹, p < 0.05). The antidiuretic hormone (ADH) concentration was also found to be lower in the CE-L trial than in the CW-H trial at the 1st and 2nd hour of recovery (p < 0.05). However, no difference was found in plasma albumin concentrations among trials throughout recovery. The results indicated that the CE solutions with higher whey protein content retained more fluid compared with CE solutions with lower whey protein content or CE solution alone. The greater fluid retention was partly caused by the elevated aldosterone concentrations in the situations of current study. / In summary, the experimental results of this thesis found that the consumption of common CE solution plus whey protein can retain more fluid in body than isocaloric CE or CE plus casein protein solution during post-exercise recovery. CE solutions with relative higher whey protein content were more effective in fluid retention than CE solutions with lower whey protein content. Furthermore, the additive effects on fluid retention caused by whey protein supplementation were induced by the increased concentrations of plasma aldosterone. The elevated plasma osmolality and ADH concentrations maybe also played a role in the greater fluid retention. However, further studies are needed to clarify this issue. The current findings provided more evidences in this research topic and suggested some recommendations to athletes and sports enthusiasts to reach rehydration rapidly and effectively after exercise. / 本論文的研究目的包括：首先，研究在普通的碳水化合物-電解質（CE）飲料中添加乳清蛋白或酪蛋白對運動後復水的影響；其次，研究CE飲料中添加不同劑量的乳清蛋白對運動後復水的影響；再次，闡述飲用CE加乳清蛋白飲料後更能有效的將水分保留在人體內的機制。 / 實驗一（第四章）研究了在CE飲料中加入一定劑量的乳清蛋白或酪蛋白對運動後復水的影響。十位年輕、健康男性受試者（平均值 ± 標準誤，年齡: 20.7 ± 0.4 歲；體重: 65.4 ± 2.0 千克；最大攝氧量: 60.7 ± 1.9 mL·kg⁻¹·min⁻¹）自願參加本項測試。按照隨機單肓交叉設計，他們完成了三次主測試，期中任何兩次測試時間都相隔七天以上。在每一次主測試中，受試者首先在跑臺上以65%最大攝氧量的運動強度完成了60分鐘的跑步運動（運動環境控制在24攝氏度，60%相對濕度），隨後開始4小時的運動後恢復階段。在恢復過程中，受試者會分別飲用三種不同飲料中的一種。三種飲料包括：（1）普通CE飲料（CE組）；（2）普通CE飲料中添加乳清蛋白（CW 組）；（3）普通CE飲料中添加酪蛋白（CC 組）。三種飲料含有相同的能量密度及電解質濃度。受試者在每次主測試中飲用的總飲料體積為1.5倍的體重減少量，這些飲料分為6等份并每隔30分鐘由受試者飲用一份。運動前、後及在恢復階段每隔一小時收集受試者的體重（裸重）、尿液樣本、及血液樣本（指尖取血）。在三次主測試中，受試者在運動結束後減少的體重量約為運動前體重的2.3%。在4小時的恢復階段中，CE組和CC組受試者排出的尿液總體積大於CW組（CE vs. CW vs. CC: 1184 ± 120 mL vs. 1005 ± 68 mL vs. 1256 ± 130 mL, p < 0.05）。所以，恢復結束後，CW組的水分保持比例高於CE組及CC組（CE vs. CW vs. CC:46.9 ± 5.2% vs. 54.9 ± 2.9% vs. 45.8 ± 5.5%, p < 0.05）。在恢復結束時，CE組的尿比重低於CW組及CC組（CE vs. CW vs. CC: 1.002 ± 0.001 g·mL⁻¹ vs. 1.004 ± 0.001g·mL⁻¹ vs. 1.004 ± 0.000 g·mL⁻¹, p < 0.05）。另外，在恢復結束後，CE組尿滲透壓水平低於CW組及CC組（CE vs. CW vs. CC: 111 ± 18 mmol·kg⁻¹ vs. 181 ± 14mmol·kg⁻¹ vs. 195 ± 23 mmol·kg⁻¹, p < 0.05）。但是，在恢復階段，血漿容量的變化在三組中沒有顯著差異。本實驗的結果表明，完成60分鐘跑步後，受試者丟失掉約2%的體重，在之後4小時恢復階段中，飲用添加乳清蛋白的CE飲料比有相同能量密度的普通CE飲料或添加酪蛋白的CE飲料更能有效的將水分保留在體內。 / 實驗二（第五章）研究了在普通CE飲料中添加不同劑量的乳清蛋白對運動後復水的影響；同時，也研究了飲用CE加乳清蛋白飲料後更能有效的將水分保留在人體內的機制。十位年輕、健康男性受試者（平均值 ± 標準誤，年齡: 22.0 ± 0.7 歲；體重: 64.5 ± 1.9 千克；最大攝氧量: 59.8 ± 1.9 mL·kg⁻¹·min⁻¹）自願參加本項測試。按照隨機單肓交叉設計，他們完成了五次主測試，任何兩次測試的時間都相隔七天以上。在每一次主測試中，受試者首先在跑臺上以65%最大攝氧量的運動強度完成了60 分鐘的跑步運動，隨後開始4 小時的運動後恢復階段。在恢復過程中，受試者會飲用五種不同飲料中的一種。五種飲料包括：（1）普通CE飲料，含有較高的CHO濃度（CE-H組）；（2）普通CE飲料，含有較低的CHO濃度（CE-L組）；（3）普通CE飲料添加較高劑量的乳清蛋白（CW-H組）；（4）普通CE飲料添加中等劑量的乳清蛋白（CW-M組）；（5）普通CE飲料添加較低劑量的乳清蛋白（CW-L組）。五種飲料含有相同濃度的電解質，其中，CE-H，CW-H，CW-M，及CW-L組有相同的能量密度，CE-L 及CW-H 組有相同的CHO含量。在每次主測試的恢復階段，受試者飲用的飲料總體積為1.5倍的體重減少量，這些飲料分為6等份并每隔30分鐘由受試者飲用一份。運動前、後及在恢復階段每隔一小時收集受試者的體重（裸重）、尿液樣本、及血液樣本（指尖取血及靜脈取血）。運動結束後，受試者的體重減少量約為運動前體重的2.2%，五組測試中沒有顯著差異。在4小時的恢復階段後，CW-M 組受試者的尿液總體積小於CE-H組（CE-H vs. CW-M:1295 ± 103 mL vs. 1049 ± 130 mL, p < 0.05）；同時，CW-H組的尿量低於CE-H，CE-L，及CW-L組（CE-H vs. CE-L vs. CW-L vs. CW-H: 1295 ± 103 mL vs. 1284 ± 90mL vs. 1141 ± 58 mL vs. 891 ± 73 mL, p < 0.01）。相對於CE-H，CE-L，及CW-L組，較少的尿液排出量使CW-M及CW-H組能將更多的水分保留在體內（CE-H vs.CE-L vs. CW-L vs. CW-M vs. CW-H: 38.4 ± 5.2% vs. 36.1 ± 4.3% vs. 43.0 ± 3.8% vs.51.0 ± 5.7% vs. 55.4 ± 3.8%, p < 0.05）。在恢復結束後，CE-H及CE-L組的尿比重水平及尿滲透壓水平低於CW-L，CW-M，及CW-H組（p < 0.05）。另外，在恢復階段的第1小時，CE-L組的血漿滲透壓水平低於CW-L，CW-M，及CW-H組（CE-L vs. CW-L vs. CW-M vs. CW-H: 274 ± 4 mmol·kg⁻¹ vs. 291 ± 4 mmol·kg⁻¹ vs. 301 ± 6 mmol·kg⁻¹ vs. 293 ± 6 mmol·kg⁻¹, p < 0.05）。在恢復階段的第2及3小時，CE-L組的血漿容量低於CW-H組；在恢復結束時，CE-L組的血漿容量低於其它四組（p <0.05）。對于兩種體液平衡調節激素，在恢復結束時，CE-H及CE-L組的醛固酮水平低於CW-M及CW-H組（CE-H vs. CE-L vs. CW-M vs. CW-H: 228 ± 100 pg·mL⁻¹ vs. 211 ± 51 pg·mL⁻¹ vs. 336 ± 85 pg·mL⁻¹ vs. 333 ± 70 pg·mL⁻¹, p < 0.05）。在恢復階段的第1及2小時，CE-L組的抗利尿激素水平低於CW-H組（p < 0.05）。然而，五組測試中，血漿白蛋白水平在恢復階段沒有顯著差異。本實驗的研究結果表明，普通CE飲料中加入較高劑量的乳清蛋白比較低劑量的乳清蛋白更能有效的將水分保留在人體內。這種較高水平的水分保留能力與醛固酮激素水平的升高有關。 / 綜上所述，本論文的研究結果發現，在運動後的恢復階段飲用添加乳清蛋白的CE飲料比有相同能量密度的普通CE飲料或添加酪蛋白的CE飲料更能有效的將水分保留在人體內。並且，在CE飲料中加入較高劑量的乳清蛋白比較低劑量的乳清蛋白對人體內水分的保留更加有效。另外，這種較高水平的水分保留能力是由醛固酮激素水平的升高引起的。同時，較高的血漿滲透壓及抗利尿激素水平可能對這種高效的水分保留能力也有一定的促進作用，但需要更多的研究來闡述這一觀點。本論文的研究結果為運動後復水的相關研究提供了更多的理論證據，並且對運動員及運動愛好者在運動結束後如何進行快速有效的復水提出了指導及建議。 / Li, Liang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2014. / Includes bibliographical references (leaves 131-149). / Abstracts also in Chinese; appendixes includes Chinese. / Title from PDF title page (viewed on 01, November, 2016). / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only.

by Chan Ping Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 108-118). / Abstracts in English and Chinese. / Abstract (in Chinese) --- p.ii / Abstract (in English) --- p.iv / Acknowledgements --- p.vii / Table of Contents --- p.viii / List of Tables --- p.xiii / List of Figures --- p.xiv / List of Appendices --- p.xv / List of Abbreviations --- p.xvi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Epidemiology of catheter associated infections --- p.1 / Chapter 1.1.1 --- Catheter associated infections --- p.1 / Chapter 1.1.2 --- Risk and mortality of CAI --- p.2 / Chapter 1.1.3 --- Etiology of CAI --- p.3 / Chapter 1.1.3.1 --- Venous catheters --- p.4 / Chapter 1.1.3.2 --- Urinary catheters --- p.4 / Chapter 1.2 --- Pathogenesis of CAI --- p.5 / Chapter 1.2.1 --- Central venous catheters (CVC) --- p.6 / Chapter 1.2.2 --- Urinary catheters --- p.7 / Chapter 1.3 --- Adhesion mechanisms --- p.7 / Chapter 1.3.1 --- Definition of adhesion --- p.7 / Chapter 1.3.2 --- Adhesion mechanism --- p.8 / Chapter 1.3.2.1 --- The phase one --- p.8 / Chapter 1.3.2.2 --- The phase two --- p.10 / Chapter 1.4 --- Catheters --- p.10 / Chapter 1.5 --- Biology of Candida albicans --- p.11 / Chapter 1.5.1 --- Taxonomy of Candida albicans --- p.11 / Chapter 1.5.2 --- Morphology --- p.12 / Chapter 1.5.3 --- Genome --- p.13 / Chapter 1.5.4 --- Biology of Candida albicans cell wall --- p.14 / Chapter 1.5.4.1 --- Constituting molecules of Candida albicans cell wall --- p.14 / Chapter 1.5.4.2 --- Organization of Candida albicans cell wall --- p.15 / Chapter 1.6 --- Agglutinin like sequence gene family --- p.16 / Chapter 1.6.1 --- Gene structure of agglutinin like sequence genes --- p.16 / Chapter 1.6.2 --- Sequence similarity --- p.17 / Chapter 1.6.3 --- Sequence variability --- p.18 / Chapter 1.6.4 --- Expression of ALS genes --- p.19 / Chapter 1.6.5 --- The Als proteins --- p.20 / Chapter 1.6.6 --- Functions of Als proteins --- p.21 / Chapter 1.7 --- Adhesion assay --- p.23 / Chapter 1.7.1 --- Adhesion model --- p.24 / Chapter 1.7.2 --- Factors affecting static adhesion model --- p.25 / Chapter 1.7.3 --- Quantitation methods of adherent cells --- p.27 / Chapter 1.7.3.1 --- Sonication --- p.27 / Chapter 1.7.3.2 --- Staining methods --- p.28 / Chapter 1.7.3.3 --- ATP bioluminescence --- p.28 / Chapter 1.8 --- Research model --- p.29 / Chapter Chapter 2 --- Aim of study --- p.31 / Chapter Chapter 3 --- Materials and Methods --- p.32 / Chapter 3.1 --- Preparation of bacteriological reagents --- p.32 / Chapter 3.2 --- Confirmation of identity of Candida albicans and of Saccharomyces cerevisiae --- p.33 / Chapter 3.3 --- Cell culture of fibroblasts --- p.36 / Chapter 3.3.1 --- Preparation of cell culture reagents --- p.36 / Chapter 3.3.2 --- Recovery of freezing fibroblasts --- p.37 / Chapter 3.3.3 --- Establishment of cell line --- p.37 / Chapter 3.4 --- Preliminary study of adherence of Candida albicans to fibroblasts and to catheters --- p.38 / Chapter 3.4.1 --- Adherence to fibroblasts --- p.38 / Chapter 3.4.1.1 --- Preparation of fibroblasts --- p.38 / Chapter 3.4.1.2 --- Preparation of culture of Candida albicans and of Saccharomyces cerevisiae --- p.39 / Chapter 3.4.1.3 --- Adhesion assay --- p.41 / Chapter 3.4.2 --- Adherence to catheters --- p.42 / Chapter 3.4.2.1 --- Preparation of catheters --- p.42 / Chapter 3.4.2.2 --- Adhesion assay --- p.42 / Chapter 3.5 --- "Confirmation of expression of ALS1, ALS5 smaller allele, and ALS6 of Candida albicans in YPD broth" --- p.44 / Chapter 3.5.1 --- RNA extraction of Candida albicans --- p.45 / Chapter 3.5.2 --- "RT-PCR of ALS1, ALS5 smaller allele, and ALS6" --- p.46 / Chapter 3.5.2.1 --- Primers --- p.46 / Chapter 3.5.2.2 --- RT-PCR --- p.47 / Chapter 3.6 --- Establishment of quantitation system of adhesion assay --- p.49 / Chapter 3.6.1 --- Absorbance measurement of Candida albicans stained with safranin --- p.49 / Chapter 3.6.1.1 --- Preparation of Candida albicans culture --- p.49 / Chapter 3.6.1.2 --- Staining of Candida albicans --- p.50 / Chapter 3.6.1.3 --- Viable count of Candida albicans adhered on the 6-well plate --- p.51 / Chapter 3.6.2 --- ATP bioluminescence --- p.52 / Chapter 3.7 --- Effect of inoculum size on adhesion to catheters --- p.53 / Chapter 3.7.1 --- Preparation of adhesion chambers --- p.53 / Chapter 3.7.2 --- Preparation of catheters --- p.54 / Chapter 3.7.3 --- Preparation of Candida albicans culture --- p.54 / Chapter 3.7.4 --- Adhesion assay --- p.55 / Chapter 3.8 --- "Transformation of Saccharomyces cerevisiae with ALS1, ALS5 smaller allele, and ALS6" --- p.57 / Chapter 3.8.1 --- DNA extraction of Candida albicans --- p.58 / Chapter 3.8.2 --- "PCR of ALS1, ALS5 smaller allele, and ALS6" --- p.59 / Chapter 3.8.3 --- Gel extraction --- p.60 / Chapter 3.8.4 --- Restriction digestion of PCR products of ALS genes and cloning plasmids --- p.61 / Chapter 3.8.5 --- "Ligation of ALS1, ALS5 smaller allele, ALS6 with pYES6CT cloning plasmids" --- p.62 / Chapter 3.8.6 --- Transformation of ligated plasmid into Escherichia coli --- p.63 / Chapter 3.8.7 --- Miniprep of plasmids --- p.64 / Chapter 3.8.8 --- DNA sequencing --- p.65 / Chapter 3.8.9 --- Transformation of Saccharomyces cerevisiae --- p.66 / Chapter 3.8.10 --- "Detection of Alsl，Als5, and Als6 protiens expression" --- p.68 / Chapter 3.8.10.1 --- Preparation of cultures in SC synthetic medium --- p.68 / Chapter 3.8.10.2 --- Protein extraction --- p.69 / Chapter 3.8.10.3 --- Dot blot of cell wall lysates --- p.69 / Chapter 3.9 --- Adhesion of transformed Saccharomyces cerevisiae to fibroblasts --- p.71 / Chapter 3.9.1 --- Preparation of fibroblasts and of Saccharomyces cerevisiae cultures --- p.71 / Chapter 3.9.2 --- Adhesion assay --- p.72 / Chapter 3.10 --- "Adhesion of transformed Saccharomyces cerevisiae to FEP, polyurethane, and silicone catheters" --- p.72 / Chapter 3.10.1 --- "Preparation of catheters, adhesion chambers and transformed Saccharomyces cerevisiae cultures" --- p.73 / Chapter 3.10.2 --- Adhesion to catheter fragments --- p.73 / Chapter 3.11 --- Statistical analysis --- p.74 / Chapter Chapter 4 --- Results --- p.75 / Chapter 4.1 --- Confirmation of identity of Candida albicans and of Saccharomyces cerevisiae --- p.75 / Chapter 4.1.1 --- Candida albicans --- p.75 / Chapter 4.1.2 --- Saccharomyces cerevisiae --- p.75 / Chapter 4.2 --- Cell culture of fibroblasts --- p.76 / Chapter 4.3 --- "Preliminary studies of adherence of Candida albicans to fibroblasts and to FEP, polyurethane, and silicone catheters" --- p.76 / Chapter 4.3.1 --- Adherence to fibroblasts --- p.76 / Chapter 4.3.2 --- Adherence to catheters --- p.77 / Chapter 4.4 --- "Confirmation of expression of ALSl, ALS5 smaller allele, and ALS6 of Candida albicans in YPD broth" --- p.78 / Chapter 4.5 --- Establishment of quantitation system of adhesion assay --- p.79 / Chapter 4.5.1 --- Absorbance measurement of Candida albicans stained with safranin --- p.79 / Chapter 4.5.2 --- ATP bioluminescence --- p.79 / Chapter 4.6 --- Effect of inoculum size on adhesion to catheters --- p.80 / Chapter 4.7 --- "Transformation of Saccharomyces cerevisiae with ALS1, ALS5 smaller allele, and ALS6" --- p.81 / Chapter 4.7.1 --- "PCR of ALSl, ALS5 smaller allele, and ALS6" --- p.81 / Chapter 4.7.2 --- Ligation of PCR products with pYES6CT plasmids --- p.82 / Chapter 4.7.3 --- "DNA sequencing results of ALS1, ALS5 smaller allele, and ALS6 ligated plasmids" --- p.83 / Chapter 4.7.4 --- "Detection of Alsl, Als5, and Als6 proteins expression" --- p.84 / Chapter 4.8 --- Adhesion of transformed Saccharomyces cerevisiae to fibroblasts --- p.84 / Chapter 4.9 --- "Adhesion of transformed Saccharomyces cerevisiae to FEP, polyurethane and silicone catheters" --- p.85 / Chapter Chapter 5 --- Discussion --- p.89 / Chapter 5.1 --- Limitations of static adhesion assay model --- p.89 / Chapter 5.2 --- Quantitation System --- p.90 / Chapter 5.2.1 --- Staining method --- p.90 / Chapter 5.2.2 --- ATP bioluminescence assay --- p.91 / Chapter 5.3 --- "Preliminary studies of adherence of Candida albicans to fibroblasts and to FEP, polyurethane, and silicone catheters" --- p.93 / Chapter 5.4 --- Effect of inoculum size on adhesion to catheters --- p.94 / Chapter 5.5 --- Selection of ALS genes --- p.96 / Chapter 5.6 --- Adhesion assay of transformed Saccharomyces cerevisiae to fibroblasts --- p.97 / Chapter 5.7 --- Adhesion assay of transformed Saccharomyces cerevisiae to catheters --- p.99 / Chapter 5.8 --- Alternative research model --- p.101 / Chapter 5.9 --- Implications and future work --- p.102 / Chapter Chapter 6 --- Conclusion --- p.107 / References --- p.108 / Tables --- p.119 / Figures --- p.123 / Appendices --- p.136