本文選題：T細(xì)胞淋巴瘤 + 瘦素��； 參考：《山東大學(xué)》2016年博士論文

【摘要】：淋巴瘤是來源于淋巴組織的惡性腫瘤,根據(jù)腫瘤細(xì)胞來源主要分為B細(xì)胞淋巴瘤和T細(xì)胞淋巴瘤(T cell lymphoma, TCL)。近年來,其發(fā)病率和死亡率逐年增加。隨著分子生物學(xué)研究的進(jìn)展,特別是酪氨酸激酶抑制劑、CD20單抗等靶向治療藥物廣泛應(yīng)用于臨床,B細(xì)胞來源的白血病、淋巴瘤的預(yù)后得到了明顯的改善。而T細(xì)胞白血�。馨土龅纳飳W(xué)行為、臨床特點(diǎn)具有高度異質(zhì)性,其發(fā)病機(jī)制尚未完全清楚,以CHOP、ESHAP為基礎(chǔ)的常規(guī)化療方案治療反應(yīng)不佳,缺少有效的分子生物學(xué)靶向治療藥物,難治、復(fù)發(fā)病例多見,預(yù)后極差。因此需要對T細(xì)胞淋巴瘤／白血病的發(fā)病的分子機(jī)制、增殖、代謝的特點(diǎn)進(jìn)行深入研究,以期為T細(xì)胞惡性腫瘤的靶向治療尋找新的方向。葡萄糖是維持機(jī)體內(nèi)環(huán)境穩(wěn)定的主要能源物質(zhì)。腫瘤細(xì)胞的增殖速度和能量消耗均明顯高于正常細(xì)胞。干擾葡萄糖攝取將會影響腫瘤細(xì)胞的增殖、代謝、侵襲能力,從而影響疾病進(jìn)展,改善疾病預(yù)后。葡萄糖轉(zhuǎn)運(yùn)蛋白(glucose transporters,Gluts)是介導(dǎo)哺乳動物細(xì)胞糖轉(zhuǎn)運(yùn)的主要載體。主要包括三類：第一類：Glut1-lut4,主要轉(zhuǎn)運(yùn)葡萄糖；第二類：Glut5, Glut7, Glut9,lut11,主要轉(zhuǎn)運(yùn)果糖；第三類：Glut6, Glut8, Glut10, Glut 12和HMIT等,功能尚不明確。在胰腺癌、胃癌、卵巢癌、宮頸癌、肺癌、鼻咽癌等腫瘤中Glut1的表達(dá)均出現(xiàn)異常增多。在原發(fā)胃的淋巴瘤中(病理類型包括彌漫大B細(xì)胞淋巴瘤和粘膜相關(guān)淋巴組織淋巴瘤),腫瘤組織表達(dá)Glut1水平與PET/CT中腫瘤攝取18FDG的SUV值明顯相關(guān)。瘦素(leptin)是一種由肥胖基因(OB)編碼的多肽類激素,主要由脂肪組織分泌,由146個(gè)氨基酸構(gòu)成,其結(jié)構(gòu)與人粒細(xì)胞刺激因子以及白介素6相似。瘦素受體(ObR)屬于I類受體家族,在人體內(nèi)存在廣泛的生物學(xué)效應(yīng)。瘦素與其受體(ObR)結(jié)合,通過JAK/STAT、PI3K/Akt和MAPK信號通路參與攝食和能量消耗、細(xì)胞增殖及凋亡以及炎癥反應(yīng)等多種病理生理過程。近年來已有大量的研究證實(shí)瘦素在多種惡性腫瘤的發(fā)生、發(fā)展過程中起重要作用。在彌漫大B細(xì)胞淋巴瘤(diffuse large B cell lymophoma, DLBCL)中,ObR的表達(dá)明顯高于反應(yīng)性增生的淋巴結(jié)組織；并且瘦素通過激活P13K/AKT信號通路促進(jìn)DLBCL細(xì)胞增殖、抑制凋亡。瘦素對機(jī)體葡萄糖代謝的影響主要是通過作用于中樞神經(jīng)系統(tǒng)和周圍組織兩個(gè)水平實(shí)現(xiàn)的。在中樞神經(jīng)系統(tǒng),瘦素作用于下丘腦神經(jīng)元,(如：葡萄糖興奮性神經(jīng)元和葡萄糖抑制性神經(jīng)元)激活細(xì)胞內(nèi)的P13K信號通路,進(jìn)而調(diào)節(jié)葡萄糖代謝。在周圍組織,瘦素主要作用于代謝相關(guān)細(xì)胞,如胰島細(xì)胞、脂肪細(xì)胞、肌肉細(xì)胞等。此外,近年來瘦素對免疫細(xì)胞,特別是活化T細(xì)胞葡萄糖代謝的影響也逐漸引起了研究者的重視。但瘦素對惡性腫瘤細(xì)胞糖代謝的作用目前僅見報(bào)道于乳腺癌細(xì)胞：高糖能促進(jìn)乳腺癌細(xì)胞表達(dá)ObR,激活瘦素信號通路,促進(jìn)其對葡萄糖的生物利用。在T細(xì)胞淋巴瘤中,瘦素對TCL細(xì)胞葡萄糖代謝和細(xì)胞增殖的作用尚未有相關(guān)研究報(bào)道,而瘦素信號通路對TCL預(yù)后的意義還不清楚。為此,我們進(jìn)行了以下兩部分實(shí)驗(yàn)：1、研究不同濃度的瘦素干預(yù)下,T細(xì)胞淋巴瘤／白血病細(xì)胞Molt-3增殖能力和葡萄糖攝取能力的變化。經(jīng)過瘦素干預(yù)后,通過提取細(xì)胞膜蛋白和Western blot法測定葡萄糖轉(zhuǎn)運(yùn)體Glut1向細(xì)胞膜轉(zhuǎn)運(yùn)情況的變化；通過RT-PCR和Western blot法檢測Glut1在mRNA和蛋白水平表達(dá)情況的變化。2、收集T細(xì)胞淋巴瘤病例的臨床資料,采用免疫組織化學(xué)法檢測ObR和Glut1在T細(xì)胞淋巴瘤組織和反應(yīng)性增生的淋巴組織中的表達(dá)情況。并對上述兩個(gè)指標(biāo)與臨床特點(diǎn)、疾病預(yù)后的相關(guān)性進(jìn)行分析。第一部分瘦素及其受體對T淋巴瘤細(xì)胞Molt-3葡萄糖攝取的影響及其機(jī)制的探討目的：葡萄糖是維持細(xì)胞生長的主要能源物質(zhì)。與正常細(xì)胞相比,腫瘤細(xì)胞具有增殖活躍,生長迅速,能量需求大的特點(diǎn)。葡萄糖代謝不僅參與腫瘤細(xì)胞增殖和凋亡的過程,還影響腫瘤預(yù)后。在急性淋巴細(xì)胞白血病中,葡萄糖代謝的抑制可以使腫瘤細(xì)胞對糖皮質(zhì)激素的殺傷作用更加敏感。瘦素(leptin)是一種蛋白質(zhì)類激素,由OB基因編碼,其結(jié)構(gòu)與生長激素、粒細(xì)胞刺激因子等相似。主要由脂肪細(xì)胞分泌,一直以來被認(rèn)為是調(diào)節(jié)機(jī)體葡萄糖代謝的重要物質(zhì)。在中樞神經(jīng)系統(tǒng),它通過與下丘腦部位相應(yīng)受體的結(jié)合,參與機(jī)體對食物攝入、能量消耗、脂肪代謝等的調(diào)節(jié)作用,維持葡萄糖穩(wěn)態(tài)。在周圍組織中,瘦素-瘦素受體-葡萄糖轉(zhuǎn)運(yùn)蛋白通路能直接作用于組織細(xì)胞,為細(xì)胞攝取利用葡萄糖的重要通路。但目前人們對瘦素在腫瘤細(xì)胞糖代謝中的作用還知之甚少。本研究選擇了人T細(xì)胞淋巴瘤細(xì)胞株Molt-3,研究瘦素及其受體對其葡萄糖代謝的影響,并探討其作用方式。材料和方法：1.TCL細(xì)胞株Molt-3與重組人瘦素共培養(yǎng)2.CCK-8測定細(xì)胞增殖3. 葡萄糖檢測試劑盒檢測細(xì)胞內(nèi)葡萄糖濃度4.提取RNA,進(jìn)行實(shí)時(shí)定量PCR5.膜蛋白、總蛋白提取以及蛋白印跡分析6.ObR特異性siRNA質(zhì)粒轉(zhuǎn)染Molt-3細(xì)胞,測定轉(zhuǎn)染后細(xì)胞內(nèi)葡萄糖濃度的變化,Western blot法測定轉(zhuǎn)染后ObR、Gluts蛋白水平的變化7.統(tǒng)計(jì)學(xué)分析結(jié)果：1.CCK-8結(jié)果顯示：隨著瘦素作用時(shí)間的延長和瘦素濃度的增加,Molt-3細(xì)胞活性逐漸增加。其差異均有統(tǒng)計(jì)學(xué)意義。2. 對細(xì)胞內(nèi)葡萄糖濃度測定結(jié)果顯示：在瘦素作用30mmin后,Molt-3細(xì)胞內(nèi)葡萄糖濃度以濃度依賴的方式增加；在瘦素作用48h后,Molt-3細(xì)胞內(nèi)葡萄糖濃度增加,其差異均具有統(tǒng)計(jì)學(xué)意義。3. Western blot結(jié)果顯示：與對照組比較,100ng/ml瘦素與Molt-3細(xì)胞共孵育30min后細(xì)胞膜蛋白中Glut1的表達(dá)水平最高,與細(xì)胞內(nèi)葡萄糖濃度的變化一致(P0.05)。4. RT-PCR與Western blot結(jié)果分別證實(shí)在瘦素作用48h后,Molt-3細(xì)胞中Glut1的mRNA和蛋白表達(dá)水平均上調(diào),而ObR和Glut4表達(dá)無明顯變化。5.ObR特異性siRNA質(zhì)粒阻斷瘦素信號通路后,ObR、Glut1蛋白表達(dá)水平下調(diào),細(xì)胞內(nèi)葡萄糖水平明顯下降。結(jié)論：1.瘦素促進(jìn)TCL細(xì)胞Molt-3細(xì)胞增殖。2.瘦素促進(jìn)Molt-3細(xì)胞攝取葡萄糖。3.瘦素對Molt-3細(xì)胞糖代謝的影響可能是通過上調(diào)Glut1的表達(dá)以及促進(jìn)Glut1募集固定于細(xì)胞膜而實(shí)現(xiàn)的。第二部分T細(xì)胞淋巴瘤中ObR和Glut1的表達(dá)情況及臨床意義目的：T細(xì)胞淋巴瘤／白血病是一組來源于T淋巴細(xì)胞的惡性腫瘤,在非霍奇金淋巴瘤(non-Hodgkin lymphoma, NHL)中占10-15%,在亞洲國家的發(fā)病率高于西方國家。與B細(xì)胞來源的腫瘤相比,T細(xì)胞淋巴瘤／白血病病情進(jìn)展快,對常規(guī)化療的反應(yīng)率不高,缺少靶向治療藥物,預(yù)后差,因此,研究T細(xì)胞惡性腫瘤的生物學(xué)特點(diǎn),以期找尋新的治療策略非常必要。瘦素參與腫瘤細(xì)胞的增殖和代謝過程,而其在T細(xì)胞淋巴瘤中的臨床意義尚不清楚。本研究收集T細(xì)胞淋巴瘤患者的臨床資料、病理標(biāo)本,研究瘦素受體ObR和葡萄糖轉(zhuǎn)運(yùn)體Glut1在T細(xì)胞淋巴瘤組織中的表達(dá)情況及其臨床意義。材料和方法：1.收集T細(xì)胞淋巴瘤患者臨床資料。2.免疫組化的方法檢測手術(shù)切除的T細(xì)胞淋巴瘤和反應(yīng)性增生的淋巴組織中CbR、Glut1、Glut4的表達(dá)情況。3. Fisher確切概率法分析ObR與其他臨床、病理指標(biāo)的相關(guān)性。4.Cox回歸法分析ObR與T細(xì)胞淋巴瘤的預(yù)后相關(guān)性。結(jié)果：1.共收集T細(xì)胞淋巴瘤病例36例。其中：外周T細(xì)胞淋巴瘤(非特指型)12例,NK/T細(xì)胞淋巴瘤8例,血管免疫母T細(xì)胞淋巴瘤3例,T免疫母細(xì)胞淋巴瘤3例,T淋巴母細(xì)胞淋巴瘤4例,間變性大細(xì)胞T細(xì)胞淋巴瘤6例。中位年齡62歲、中位生存期16.5個(gè)月,3年生存率14.0%。2.T細(xì)胞淋巴瘤組織中ObR和Glut1的表達(dá)率高于反應(yīng)性增生的淋巴結(jié)組織(58.3% vs 22.2%, P=0.012),而Glut4在二者中的表達(dá)情況無統(tǒng)計(jì)學(xué)差異。3.ObR的表達(dá)情況與與Glut1表達(dá)存在相關(guān)性(P=0.007),與Glut4表達(dá)不相關(guān)(P=0.292),并且與患者的年齡、性別、分期、LDH水平、B癥狀、合并糖尿病等亦不相關(guān)。4.單因素分析顯示：年齡大于60歲以及共同表達(dá)ObR、Glut1者預(yù)后不良,多因素分析提示：共同表達(dá)ObR、Glut1為影響T細(xì)胞淋巴瘤預(yù)后的獨(dú)立危險(xiǎn)因素(HR=3.420,95%CI 1.293-9.049, P=0.013)結(jié)論：1.ObR和Glut1在T細(xì)胞淋巴瘤組織中的表達(dá)高于反應(yīng)性增生的淋巴結(jié)組織。2.在細(xì)胞淋巴瘤組織中ObR和Glut1的表達(dá)存在相關(guān)性。3.T細(xì)胞淋巴瘤預(yù)后差,在T細(xì)胞淋巴瘤中,共同表達(dá)ObR和Glut1為獨(dú)立的不良預(yù)后因素。
[Abstract]:Lymphoma is a malignant tumor derived from lymphoid tissue, which is mainly divided into B cell lymphoma and T cell lymphoma (T cell lymphoma, TCL) based on the source of tumor cells. In recent years, its incidence and mortality have increased year by year. With the progress of molecular biology research, especially tyrosine kinase inhibitors, CD20 McAbs, and other targeted therapies. The prognosis of B cell leukemia and lymphoma has been significantly improved in clinical use. The biological behavior and clinical characteristics of T cell leukemia / lymphoma are highly heterogeneous, its pathogenesis is not completely clear, and the conventional chemotherapy based on CHOP and ESHAP is not effective and lacks effective molecular biological targets. It is necessary to study the molecular mechanism, proliferation and metabolism of T cell lymphoma / leukemia, so as to find a new direction for the targeting therapy of T cell malignant tumor. The proliferation rate and energy consumption are significantly higher than that of normal cells. Interference with glucose uptake will affect the proliferation, metabolism and invasiveness of tumor cells, which affect the progression of the disease and improve the prognosis of the disease. Glucose transporter (glucose transporters, Gluts) is the main carrier of sugar transport in mammalian cells. It mainly includes three types: First class: Glut1-lut4, mainly transporting glucose; second types: Glut5, Glut7, Glut9, lut11, mainly transporting fructose; the third types: Glut6, Glut8, Glut10, Glut 12 and HMIT, etc. the function is not yet clear. The Glut1 expression in pancreatic, gastric, ovarian, cervical, cervical, nasopharyngeal cancer and other tumors. The pathological types include diffuse large B cell lymphoma and mucosa associated lymphoid tissue lymphoma. The expression of Glut1 in tumor tissue is significantly related to the SUV value of 18FDG in PET/CT. Leptin (leptin) is a polypeptide hormone encoded by the obesity gene (OB), which is mainly secreted by adipose tissue and consists of 146 amino acids. It is similar to human granulocyte stimulating factor and interleukin 6. Leptin receptor (ObR) belongs to the I receptor family, and has extensive biological effects in human body. Leptin and its receptor (ObR) are combined with JAK/STAT, PI3K/Akt and MAPK signaling pathways to participate in feeding and energy consumption, cell proliferation and apoptosis, and inflammatory reactions. In recent years, a large number of studies have shown that leptin plays an important role in the development of a variety of malignant tumors. In the diffuse large B cell lymphoma (diffuse large B cell lymophoma, DLBCL), the expression of ObR is significantly higher than the reactive proliferation of lymph nodes; and leptin promotes DLBCL by activating the P13K/AKT signaling pathway. The effect of leptin on the metabolism of glucose is realized mainly by two levels of the central nervous system and the surrounding tissue. In the central nervous system, leptin acts on the hypothalamic neurons, such as glucose excitatory neurons and glucose suppressor neurons, to activate the P13K signaling pathway in the cells. In the surrounding tissue, leptin mainly acts on metabolic related cells, such as islet cells, adipocytes, and muscle cells. In addition, the effect of leptin on the metabolism of glucose in immune cells, especially in activated T cells, has gradually aroused the attention of researchers in recent years. It is only reported in breast cancer cells: high glucose can promote the expression of ObR in breast cancer cells, activate leptin signaling pathway and promote the biological utilization of glucose. In T cell lymphoma, the effect of leptin on glucose metabolism and cell proliferation in TCL cells has not been reported, but the significance of leptin signaling pathway to the prognosis of TCL is not yet significant. To this end, we conducted the following two experiments: 1, to study the changes in the proliferation and glucose uptake of T cell lymphoma / leukemia cells under the intervention of different concentrations of leptin. After leptin intervention, the transport of glucose transporter Glut1 into the cell membrane was determined by the extraction of cell membrane protein and Western blot method. The changes in the expression of Glut1 in mRNA and protein levels were detected by RT-PCR and Western blot. The clinical data of the cases of T cell lymphoma were collected. The expression of ObR and Glut1 in T cell lymphoma and reactive proliferation of lymphoid tissues was detected by immunohistochemistry. The above two indexes and clinical manifestations were observed. Characteristics, analysis of the correlation between the prognosis of the disease. Part 1 the effect of leptin and its receptor on the uptake of Molt-3 glucose in T lymphoma cells and its mechanism: glucose is the main source of energy for the maintenance of cell growth. Compared with normal cells, the tumor cells have the characteristics of active proliferation, rapid growth and large energy demand. Glucose metabolism not only participates in the process of tumor cell proliferation and apoptosis, but also affects the prognosis of the tumor. In acute lymphoblastic leukemia, the inhibition of glucose metabolism can make the tumor cells more sensitive to the killing of glucocorticoids. Leptin is a kind of protein irritable, encoded by the OB gene, and its structure and growth hormone are fine. It is believed to be an important substance that regulates the metabolism of glucose in the body. In the central nervous system, it participates in the regulation of food intake, energy consumption, fat metabolism and so on by combining with the corresponding receptors in the hypothalamus to maintain the glucose homeostasis. In the fabric, leptin leptin receptor glucosglucose transporter pathway can directly act on tissue cells, and it is an important pathway for the uptake of glucose in cells. However, little is known about the role of leptin in the glucose metabolism of tumor cells. This study selected human T cell lymphoma cell line Molt-3 and studied leptin and its receptor to its glucose. The effects of metabolism and methods of action. Materials and methods: 1.TCL cell line Molt-3 and recombinant human leptin co culture 2.CCK-8 determination of cell proliferation 3. glucose detection kit to detect intracellular glucose concentration 4. extract RNA, real-time quantitative PCR5. membrane protein, total protein extraction and Western blot analysis of 6.ObR specific siRNA plasmid Molt-3 cells were transfected to determine the changes of glucose concentration in the cells after transfection. Western blot assay was used to determine ObR after transfection. The changes of Gluts protein level were 7. statistical analysis results: 1.CCK-8 results showed that the activity of Molt-3 cells increased gradually with the prolongation of the action time of leptin and the increase of leptin concentration. The difference was statistically significant.2. The results of intracellular glucose concentration measurement showed that after leptin action 30mmin, the glucose concentration in Molt-3 cells increased in a concentration dependent manner, and the glucose concentration in Molt-3 cells increased after leptin action 48h, and the difference was statistically significant.3. Western blot results showed that 100ng/ml leptin and Molt were compared with the control group. The expression level of Glut1 in the membrane protein of -3 cells was the highest, which was the same as that of the intracellular glucose concentration (P0.05). (P0.05).4. RT-PCR and Western blot results showed that the Glut1 mRNA and protein expression level in Molt-3 cells increased after the action of leptin, respectively. After the plasmid blocked the leptin signaling pathway, the expression level of ObR, Glut1 protein was down, and the glucose level in cells decreased significantly. Conclusion: 1. leptin promotes the proliferation of.2. leptin in Molt-3 cells of TCL cells and promotes the uptake of glucose.3. leptin by Molt-3 cells to the glucose metabolism of Molt-3 cells by up regulating the expression of Glut1 and promoting Glut1 recruitment. The expression of ObR and Glut1 in second part of T cell lymphoma and its clinical significance: T cell lymphoma / leukemia is a group of malignant tumors derived from T lymphocyte, which accounts for 10-15% in non Hodgkin lymphoma (non-Hodgkin lymphoma, NHL), and the incidence in Asian countries is higher than that in western countries. Compared with the tumor derived from B cells, T cell lymphoma / leukemia progress rapidly, the response rate of conventional chemotherapy is not high, the target therapy drug is short, the prognosis is poor. Therefore, it is necessary to study the biological characteristics of T cell malignant tumor in order to find new treatment strategies. Leptin is involved in the proliferation and metabolic process of tumor cells, and it is in T. The clinical significance of cell lymphoma is still unclear. This study collects the clinical data of T cell lymphoma patients, pathological specimens, and studies the expression and clinical significance of leptin receptor ObR and glucose transporter Glut1 in T cell lymphoma tissue. Materials and methods: 1. the immunohistochemical staining of the clinical data of T cell lymphoma patients was collected by.2. Methods to detect the expression of CbR, Glut1, Glut4 in surgical excised T cell lymphoma and reactive proliferative lymphoid tissue,.3. Fisher accurate probability analysis of ObR and other clinical and pathological indexes, correlation.4.Cox regression analysis of the prognostic correlation between ObR and T cell lymphoma. 36 cases of T cell lymphoma were collected in 1. cases. 12 cases of peripheral T cell lymphoma (non special type), 8 cases of NK/T cell lymphoma, 3 cases of angioimmuno T cell lymphoma, 3 cases of T immunblastial lymphoma, 4 cases of T lymphoblastic lymphoma and 6 cases of T cell lymphoma of anaplastic large cells. The median age is 62, the median survival time is 16.5 months, and the 3 year survival rate of 14.0%.2.T cell lymphoma tissue is ObR. The expression rate of and Glut1 was higher than that of reactive hyperplasia (58.3% vs 22.2%, P=0.012), and there was no statistical difference in the expression of Glut4 in the two. The expression of.3.ObR was correlated with the expression of Glut1 (P=0.007), not associated with the expression of Glut4 (P=0.292), and was associated with the patient's age, sex, stage, LDH level, B symptoms. Diabetes and other unrelated.4. analysis showed that age is more than 60 years old and co expression of ObR and Glut1 has poor prognosis. Multivariate analysis suggests that common expression of ObR, Glut1 as an independent risk factor for the prognosis of T cell lymphoma (HR=3.420,95%CI 1.293-9.049, P=0.013): 1.ObR and Glut1 in T cell lymphoma tissue The expression of ObR and Glut1 in lymphoid tissue, which is higher than reactive hyperplasia, has a poor prognosis for the expression of.3.T cell lymphoma. In T cell lymphoma, the common expression of ObR and Glut1 is an independent prognostic factor in T cell lymphoma.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R733.1

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 繆明永;楊生生;陳歡;高云;張建鵬;;以葡萄糖代謝為中心開展物質(zhì)代謝教學(xué)體會[J];基礎(chǔ)醫(yī)學(xué)教育;2013年07期

2 鄭景略;;鸚鵡熱-沙眼組病原體的葡萄糖代謝[J];醫(yī)學(xué)文摘(眼科學(xué));1965年03期

3 黃泳,唐安戊,李求實(shí),李東江,夏東斌,解亞寧;頭針對正常人和抑郁癥患者顳葉葡萄糖代謝的影響[J];江蘇中醫(yī)藥;2004年10期

4 張雪竹;劉存志;于建春;丁曉蓉;韓景獻(xiàn);;腦組織葡萄糖代謝的研究方法[J];國際腦血管病雜志;2006年10期

5 侯志敏;;2型糖尿病中葡萄糖代謝異常的研究進(jìn)展[J];廊坊師范學(xué)院學(xué)報(bào)(自然科學(xué)版);2009年02期

6 張昊文;劉建軍;馮爽;徐媛媛;蔣昕;劉芬菊;;腫瘤細(xì)胞~3H-葡萄糖代謝測量方法的建立[J];蘇州大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2011年01期

7 劉宇;汪魯華;古麗扎爾·買買提明;;阻塞性睡眠呼吸暫停綜合征患者葡萄糖代謝研究[J];中華實(shí)用診斷與治療雜志;2011年02期

8 周永華;黃洪波;陶永輝;俞惠新;許永良;張英;高琪;;弓形蟲慢性感染對小鼠腦內(nèi)葡萄糖代謝影響的研究[J];中國血吸蟲病防治雜志;2011年03期

9 王榮f;;結(jié)、直腸癌的葡萄糖周轉(zhuǎn)和再循環(huán)[J];國外醫(yī)學(xué)(消化系疾病分冊);1984年04期

10 黃泳,唐安戊,李東江,夏東斌,李求實(shí);頭針對正常人和抑郁癥患者丘腦葡萄糖代謝的影響[J];新中醫(yī);2004年10期

相關(guān)會議論文 前10條

1 唐天奕;李延兵;賈偉平;包玉倩;項(xiàng)坤三;翁建平;;A型胰島素抵抗綜合征個(gè)體葡萄糖代謝初步研究[A];2006年中華醫(yī)學(xué)會糖尿病分會第十次全國糖尿病學(xué)術(shù)會議論文集[C];2006年

2 郭誼;王爽;高峰;丁美萍;;重復(fù)經(jīng)顱磁刺激對大鼠各腦區(qū)葡萄糖代謝作用的頻率依賴性[A];2009年浙江省神經(jīng)病學(xué)學(xué)術(shù)年會論文匯編[C];2009年

3 張瓊月;苗青;葉紅英;張朝云;薛瑞丹;朱小明;李益明;左傳濤;管一暉;;腦區(qū)葡萄糖代謝與健康成人棕色脂肪活性的關(guān)系[A];中華醫(yī)學(xué)會第十二次全國內(nèi)分泌學(xué)學(xué)術(shù)會議論文匯編[C];2013年

4 唐麗;高率斌;栗夏蓮;;血管緊張素Ⅱ?qū)epG2細(xì)胞葡萄糖代謝的影響及纈沙坦的干預(yù)作用[A];中華醫(yī)學(xué)會第十二次全國內(nèi)分泌學(xué)學(xué)術(shù)會議論文匯編[C];2013年

5 薛承銳;李珊珊;趙占朝;梁泉;袁泳;李偉;;肝瘀癥大鼠肝臟葡萄糖代謝和肝纖維化的變化[A];第五次全國中西醫(yī)結(jié)合血瘀證及活血化瘀研究學(xué)術(shù)大會論文匯編[C];2001年

6 楊洪文;周平;馬黎明;洪愉;趙繼華;陳翼;李亞松;;利用葡萄糖代謝均勻程度評價(jià)肺部實(shí)性結(jié)節(jié)的良惡性[A];首屆全國分子核醫(yī)學(xué)暨分子影像學(xué)學(xué)術(shù)交流會資料匯編[C];2006年

7 左傳濤;;SPM的基本原理及應(yīng)用[A];全國神經(jīng)核醫(yī)學(xué)與神經(jīng)科學(xué)新進(jìn)展研討會暨核醫(yī)學(xué)科普專家工作會議資料匯編[C];2007年

8 張超;唐麗娜;鄧姍姍;相莉;孫洪范;;胰島素治療對四氧嘧啶糖尿病小鼠口服葡萄糖代謝的影響[A];天津市生物醫(yī)學(xué)工程學(xué)會第29屆學(xué)術(shù)年會暨首屆生物醫(yī)學(xué)工程前沿科學(xué)研討會論文集[C];2009年

9 牛義民;王華;劉達(dá)興;徐剛;;犬SMC后心臟葡萄糖代謝變化[A];貴州省醫(yī)學(xué)會胸心血管外科分會2010年學(xué)術(shù)年會論文集[C];2010年

10 張蕾;廖秦平;;睪酮和二甲雙胍對子宮內(nèi)膜葡萄糖代謝的影響[A];中華醫(yī)學(xué)會第一屆全球華人婦產(chǎn)科學(xué)術(shù)大會暨第三次全國婦產(chǎn)科中青年醫(yī)師學(xué)術(shù)會議論文匯編[C];2007年

相關(guān)重要報(bào)紙文章 前6條

1 北京大學(xué)醫(yī)學(xué)博士 趙承淵;1947：葡萄糖與女性科學(xué)家[N];東方早報(bào);2013年

2 記者 顧淑霞;清華顏寧研究組取得生命科學(xué)基礎(chǔ)研究重大突破[N];新清華;2014年

3 賈少微;王全師;應(yīng)用PET研究針刺信號對人腦的影響[N];中國醫(yī)藥報(bào);2003年

4 南方日報(bào)記者 曹斯　實(shí)習(xí)生 趙莞 通訊員 溫志勤 策劃統(tǒng)籌 徐林 殷劍鋒;“大塊頭”有大本領(lǐng)[N];南方日報(bào);2013年

5 靖九江;轉(zhuǎn)化糖輸液的臨床優(yōu)勢[N];中國醫(yī)藥報(bào);2004年

6 陶海;哪些眼病需要做PET檢查[N];家庭醫(yī)生報(bào);2006年

相關(guān)博士學(xué)位論文 前7條

1 王增敏;氧化還原調(diào)控在皮質(zhì)醇調(diào)節(jié)肝細(xì)胞內(nèi)質(zhì)網(wǎng)葡萄糖代謝的機(jī)制研究[D];山東大學(xué);2016年

2 韓天潔;瘦素信號通路對T淋巴瘤細(xì)胞葡萄糖代謝的影響及其臨床意義[D];山東大學(xué);2016年

3 高峰;小動物PET在癲癇和腦缺血模型中的應(yīng)用研究[D];浙江大學(xué);2009年

4 陳巧珍;基于PET分子影像的注意功能研究[D];浙江大學(xué);2013年

5 楊映娟;Fyn在小鼠肝臟葡萄糖代謝中的作用及機(jī)理研究[D];西北農(nóng)林科技大學(xué);2014年

6 周閃;PET定量分析方法研究[D];鄭州大學(xué);2013年

7 李學(xué)智;電針少陽經(jīng)穴對偏頭痛患者腦內(nèi)葡萄糖代謝影響的研究[D];成都中醫(yī)藥大學(xué);2009年

相關(guān)碩士學(xué)位論文 前10條

1 何亞非;MicroRNA126對人正常肝細(xì)胞葡萄糖代謝的影響[D];鄭州大學(xué);2015年

2 孔凡華;釀酒酵母葡萄糖耐量因子對脂肪細(xì)胞葡萄糖代謝的影響[D];天津大學(xué);2014年

3 劉丹丹;PI3K-Akt信號通路在葡萄糖誘導(dǎo)的鵝肝細(xì)胞脂質(zhì)合成中的作用研究[D];四川農(nóng)業(yè)大學(xué);2014年

4 王華;開放式犬SMC模型的建立及SMC后心臟葡萄糖代謝變化[D];遵義醫(yī)學(xué)院;2010年

5 袁倩;葡萄糖對INS-1細(xì)胞PTEN和P-AKT表達(dá)的影響[D];復(fù)旦大學(xué);2010年

6 宋盼愛;PKCδ對高葡萄糖誘導(dǎo)的HK-2細(xì)胞p66Shc磷酸化及線粒體轉(zhuǎn)位的影響[D];中南大學(xué);2013年

7 于平;基于微透析技術(shù)的葡萄糖檢測系統(tǒng)[D];浙江大學(xué);2001年

8 張旭;葡萄糖專一性磷酸轉(zhuǎn)移酶系統(tǒng)單基因缺失對大腸桿菌生理特性的影響[D];山東大學(xué);2014年

9 李倩延;氧化葡萄糖桿菌（Gluconobacter oxydans）DHA3-9菌株葡萄糖酸轉(zhuǎn)化及葡萄糖代謝酶系的研究[D];浙江大學(xué);2013年

10 葛衛(wèi)寧;葡萄糖對血管內(nèi)皮細(xì)胞一氧化氮釋放及內(nèi)皮型一氧化氮合酶活性的影響[D];青島大學(xué);2008年

，

本文編號：1972850