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葡萄糖短缺對大鼠視叉上核中樞時鐘膜興奮性與胞內鈣離子的作用

為了解決cx-5 2024的問題，作者鄭若喬 這樣論述：

Table of Contents指導教授推薦書口試委員會審定書致謝中文摘要 ............................................................iAbstract ...........................................................ivTable of Contents .................................................viiList of Figures ...........................................

.........ixChapter 1. Introduction .............................................11. The central clock of the suprachiasmatic nucleus (SCN) ......11-1 The anatomical and morphological features .......................11-2 Molecular clockwork in mammals ..................................11-3 Afferen

t projections ............................................31-4 Efferent projections ............................................31-5 Rhythmicity of electrical activities and [Ca2+]i ................42. Energy metabolism affects phase shift on the SCN ............63. Glucose sensitivity and hom

eostasis in the brain ............63-1 Glucose sensing in the central nervous system ...................63-2 Glucose sensing in the SCN ......................................83-3 The metabolic molecular candidates in the SCN neurons ..........103-3-1 ATP-sensitive K+ (KATP) channel .................

.............103-3-2 Na/K pump (Na+ pump; NKA) ....................................104. Metabolic regulation of ionic homeostasis in the SCN .......115. Specific aims ..............................................13Chapter 2. Materials and Methods ...................................141. Hyp

othalamic brain slice and reduced SCN preparation .......142. Electrical recordings ......................................153. Ca2+ and Na+ imaging .......................................164. Drugs ......................................................18Chapter 3. Metabolic regulation of me

mbrane excitability in the dSCN neurons ............................................................19Results ............................................................19Discussion .........................................................26Chapter 4. Metabolic regulation of [Ca2+]i homeostasis in

the SCN neurons ............................................................32Results ............................................................32Discussion .........................................................45Chapter 5. Metabolic regulation of glutamate-evoked Ca2+ responses in the SCN neur

ons ....................................................52Results ............................................................52Discussion .........................................................59Chapter 6. Conclusion ..............................................62Figures ........................

....................................64References ........................................................100List of FiguresFig. 3-1 Glucoprivation produces biphasic effect on spontaneous firing ....................................................................64Fig. 3-2 Summary of glucoprivation-i

nduced early excitation and delayed inhibition on firing in dSCN and vSCN neurons ..............65Fig. 3-3 Glucoprivation-induced inhibition of firing is mediated by opening of the KATP channel on the dSCN neurons ....................66Fig. 3-4 Summary of glucoprivation-induced inhibition on dSCN an

d vSCN neurons ............................................................67Fig. 3-5 Firing responses to hypoglycemia on the SCN neuron ........68Fig. 3-6 Hypoglycemia selectively inhibits the K ATP-expressing SCN neuron .............................................................69Fig. 3-7 Summar

y of hypoglycemia-induced firing inhibition in the KATP-expressing and KATP-non-expressing SCN neurons ................70Fig. 4-1 Effects of glucoprivation on the basal [Ca2+]i in the dSCN and vSCN ...........................................................71Fig. 4-2 Effects of glucoprivation on 20

K+-evoked Ca2+ transients .73Fig. 4-3 Effects of hypoglycemia on 20 K+-evoked Ca2+ transients ...75Fig. 4-4 Effects of pre-incubation with hypoglycemia on 20 K+-evoked Ca2+ transients ....................................................77Fig. 4-5 Effects of hypoglycemia and glucoprivation on [Na+]i

......79Fig. 4-6 Effects of 1 μM ouabain on 20 K+-evoked Ca2+ transients ...80Fig. 4-7 Effects of 10 μM ouabain on 20 K+-evoked Ca2+ transients ..82Fig. 4-8 Preferential enhancement by glucose shortage of nimodipine-insensitive Ca2+ transients ........................................84Fig. 5-1 Kinet

ic differences between Ca2+ responses to 20 mM K+ and 100 µM glutamate ...................................................86Fig. 5-2 Effects of glucoprivation on glutamate-evoked Ca2+ responses ....................................................................88Fig. 5-3 Effects of hypoglycemia on

glutamate-evoked Ca2+ responses ....................................................................90Fig. 5-4 Effects of pre-incubation with hypoglycemia on glutamate-evoked Ca2+ responses ..............................................92Fig. 5-5 Comparable effects on [Ca2+]i and [Na+]i response to

0-K+ andglutamate ..........................................................94Fig. 5-6 Inhibition of OXPHOS effects on glutamate-evoked Ca2+responses ..........................................................96Fig. 5-7 1 µM ouabain effects on glutamate-evoked Ca2+ responses ...98

探討抗聚乙二醇抗體對聚乙二醇修飾紅血球生成素藥物活性的影響

為了解決cx-5 2024的問題，作者張恬菁 這樣論述：

聚乙二醇（PEG）是合成的水溶性聚合物，廣泛用於日用品和生物製藥中。 PEG與生物分子的結合可以延長其在血液中的循環時間。PEG被認為是非免疫原性的，但是最近的報告顯示，在臨床試驗和動物研究中，通過注射某些類型的聚乙二醇修飾微脂體或蛋白質來誘導抗聚乙二醇抗體。儘管大多數施以聚乙二醇修飾蛋白治療的患者並未誘導出抗聚乙二醇抗體，但從未接觸過聚乙二醇修飾藥物的健康個體中有很大一部分在其血液中已存在抗聚乙二醇抗體。根據統計，約40％的健康個體中存在抗聚乙二醇抗體。然而，尚不清楚抗聚乙二醇抗體是否會影響美血樂（Mircera，甲氧基聚乙二醇修飾紅血球生成素β）的生物活性，美血樂是紅血球生成刺激素（ES

A），用於治療與慢性腎臟病相關的貧血患者。我們發現健康個體血清中存在的抗聚乙二醇抗體可以與美血樂結合。藉由分析JAK2和STAT5的磷酸化，我們發現抗聚乙二醇單株抗體IgM和IgG在高濃度下均可改變美血樂對紅血球生成素受體信號傳導，進而降低UT-7人類白血病細胞增生。小鼠中的抗聚乙二醇IgM和IgG抗體隨劑量增加，從血液循環中清除放射性碘標記的美血樂也隨之增加，從而導致美血樂刺激紅血球生成的效力降低。同時，具有不同親和力的抗聚乙二醇抗體亦改變了清除美血樂的藥物動力學。經由抗聚乙二醇抗體IgG清除美血樂是由抗體的Fc部分調控，且清除的美血樂主要積聚在小鼠的肝臟和脾臟中。抗聚乙二醇抗體對美血樂生物

活性的抑制作用可以藉由在小鼠中注射更高劑量的美血樂來抵銷。在對美血樂反應較差的透析患者中，我們也發現帶有抗聚乙二醇抗體的比例和濃度皆較高。我們的研究結果顯示，帶有較多抗聚乙二醇抗體的患者中，美血樂的生物活性和治療效力可能會降低。