激動(dòng)HepG2細(xì)胞β3-AR對(duì)泡沫細(xì)胞荷脂過程影響及PCI和CABG術(shù)后患者心血管危險(xiǎn)因素達(dá)標(biāo)現(xiàn)狀的研究
本文選題:激動(dòng) + HepG2; 參考:《首都醫(yī)科大學(xué)》2017年博士論文
【摘要】:背景動(dòng)脈粥樣硬化(atherosclerosis,AS)引起的心腦血管疾病是引起人類死亡的頭號(hào)殺手。泡沫細(xì)胞的形成是AS早期的標(biāo)志之一,也是AS發(fā)生、發(fā)展的關(guān)鍵步驟。泡沫細(xì)胞形成的主要原因是巨噬細(xì)胞內(nèi)膽固醇流入和流出的失衡。因此,促進(jìn)泡沫細(xì)胞內(nèi)膽固醇流出能夠抑制泡沫細(xì)胞的形成,延緩動(dòng)脈粥樣硬化病變的發(fā)生與發(fā)展。膽固醇逆轉(zhuǎn)運(yùn)(RCT)是指HDL將多余的膽固醇從周圍組織(包括動(dòng)脈粥樣斑塊)、細(xì)胞轉(zhuǎn)運(yùn)到肝臟進(jìn)行機(jī)體的再循環(huán)或以膽酸的形式排出體外,這一過程包括組織細(xì)胞膽固醇的流出至細(xì)胞外受體(如HDL)、膽固醇的酯化以及清除。近來,如何促進(jìn)巨噬細(xì)胞RCT成為抗動(dòng)脈粥樣硬化研究的熱點(diǎn)。β3-AR最早被發(fā)現(xiàn)于1980年,主要在白色和棕色脂肪組織表達(dá),近年研究發(fā)現(xiàn)其在心臟、腦、肺臟及肝臟等組織也有表達(dá)。本課題組近年的研究發(fā)現(xiàn),激動(dòng)Apo E-/-小鼠β3-AR能夠改善血脂代謝紊亂,降低TC、VLDL/LDL-C和TG,升高HDL;促進(jìn)膽固醇經(jīng)膽汁及糞便排出;縮小胸主動(dòng)脈動(dòng)脈粥樣硬化斑塊面積,由此推斷β3-AR可能通過促進(jìn)膽固醇逆轉(zhuǎn)運(yùn)起到抗動(dòng)脈粥樣硬化作用。本研究使用β3-AR激動(dòng)劑與拮抗劑刺激Hep G2細(xì)胞,觀察其上清液對(duì)RAW264.7巨噬細(xì)胞源性泡沫細(xì)胞內(nèi)脂質(zhì)及膽固醇流出的影響,探索β3-AR對(duì)RCT的影響及其可能機(jī)制,為臨床開發(fā)新型抗動(dòng)脈硬化藥物提供理論依據(jù)。目的通過激動(dòng)或抑制Hep G2細(xì)胞的β3-AR,觀察其分泌蛋白對(duì)巨噬細(xì)胞源性泡沫細(xì)胞荷脂過程的影響,探索β3-AR調(diào)節(jié)膽固醇逆轉(zhuǎn)運(yùn)(RCT)過程的可能機(jī)制。方法使用β3-AR激動(dòng)劑(BRL37344)和β3-AR拮抗劑(SR52390A)分別刺激培養(yǎng)的Hep G2細(xì)胞,Elisa法檢測(cè)上清液Apo A-I、Apo A-II、Apo B及β3-AR含量;實(shí)時(shí)定量PCR和蛋白印跡法分別檢測(cè)細(xì)胞內(nèi)Apo A-I、Apo A-II、Apo B、β3-AR、PPARγ及PPARα含量;以ac-LDL(50μg/m L)誘導(dǎo)巨噬細(xì)胞源性泡沫細(xì)胞形成,收集Hep G2各組細(xì)胞上清液,加入巨噬細(xì)胞源性泡沫細(xì)胞共同孵育,采用油紅O染色進(jìn)行細(xì)胞形態(tài)學(xué)觀察,酶法測(cè)定細(xì)胞內(nèi)總膽固醇(TC)、游離膽固醇(FC)和膽固醇酯(CE)水平,3H標(biāo)記的膽固醇測(cè)定膽固醇流出率,蛋白印跡法檢測(cè)細(xì)胞中ABCA1和ABCG1的表達(dá)。結(jié)果1、對(duì)Hep G2細(xì)胞進(jìn)行Elisa檢測(cè)結(jié)果表明,與空白對(duì)照組相比,BRL37344組Apo A-I水平顯著升高(P0.01),SR59230A組Apo A-I水平顯著降低(P0.01);與空白對(duì)照組相比,BRL37344組Apo A-II含量顯著降低(P0.01),SR59230A組Apo A-II水平無顯著性差異(P0.05);Apo B水平在三組上清液中無顯著性差異(P0.05)。2、RT-PCR結(jié)果表明,與空白對(duì)照組相比,BRL37344組Apo A-I m RNA水平顯著升高(P0.01),SR59230A組Apo A-I m RNA水平顯著降低(P0.01);與空白對(duì)照組相比,BRL37344組Apo A-II m RNA水平顯著降低(P0.01),SR59230A組Apo A-II m RNA水平無顯著性差異(P0.05);與空白對(duì)照組相比,BRL37344組β3-AR m RNA水平顯著升高(P0.01),SR59230A組β3-AR m RNA水平顯著降低(P0.01);Apo B水平在三組中無顯著性差異(P0.05)。Apo A-I,Apo A-II和Apo B蛋白表達(dá)水平與m RNA表達(dá)情況相同。3、BRL37344刺激顯著上調(diào)Hep G2細(xì)胞中PPARγ的表達(dá)(P0.01),但不增加Hep G2細(xì)胞中PPARα的表達(dá)(P0.05),SR59230A刺激使Hep G2細(xì)胞中PPARγ的表達(dá)水平顯著下調(diào)(P0.01),對(duì)PPARα的表達(dá)無影響(P0.05)。BRL37344刺激引起的Apo AI蛋白表達(dá)上調(diào)效應(yīng)可被PPARγ拮抗劑GW9662所阻斷(P0.01)。4、酶法檢測(cè)結(jié)果表明,與空白對(duì)照組相比,BRL37344組細(xì)胞內(nèi)TC、CE水平顯著降低(P均0.05),SR59230A組細(xì)胞內(nèi)TC、CE水平顯著升高(P均0.05);與空白對(duì)照組相比,BRL37344組細(xì)胞內(nèi)FC水平顯著升高(P0.01),SR59230A組細(xì)胞內(nèi)FC水平無顯著差異(P0.05)。5、與空白對(duì)照組相比,BRL37344刺激的Hep G2細(xì)胞上清液顯著上調(diào)巨噬細(xì)胞內(nèi)ABCA1蛋白的表達(dá)(P0.01);SR59230A組ABCA1蛋白的表達(dá)無顯著性差異(P0.05);巨噬細(xì)胞內(nèi)ABCG1蛋白表達(dá)在三組之間無顯著性差異(P0.05)。結(jié)論1.激動(dòng)β3-AR明顯上調(diào)Hep G2細(xì)胞內(nèi)Apo A-I蛋白水平表達(dá);2.激動(dòng)β3-AR顯著上調(diào)Hep G2細(xì)胞內(nèi)PPARγ蛋白的表達(dá);3.激動(dòng)β3-AR對(duì)Hep G2細(xì)胞內(nèi)Apo A-I蛋白表達(dá)的上調(diào)可能依賴PPARγ途徑;4.β3-AR激動(dòng)后的Hep G2細(xì)胞上清液能夠促進(jìn)巨噬細(xì)胞源性泡沫細(xì)胞內(nèi)膽固醇流出。5.β3-AR激動(dòng)后的Hep G2細(xì)胞上清液可能通過ABCA1途徑促進(jìn)泡沫細(xì)胞內(nèi)膽固醇流出。背景二級(jí)預(yù)防藥物的使用能夠?yàn)檠\(yùn)重建患者帶來臨床獲益,比較經(jīng)皮冠狀動(dòng)脈介入和冠狀動(dòng)脈搭橋患者術(shù)后二級(jí)預(yù)防藥物的使用、血脂、血壓及血糖達(dá)標(biāo)率及終點(diǎn)事件發(fā)生率情況的研究鮮見報(bào)道。目的通過對(duì)PCI和CABG術(shù)后患者二級(jí)預(yù)防藥物使用、血脂、血壓及血糖達(dá)標(biāo)率及終點(diǎn)事件發(fā)生率的分析比較,探討PCI和CABG術(shù)后患者心血管相關(guān)危險(xiǎn)因素控制情況是否存在差異及對(duì)預(yù)后的影響。方法回顧性分析2014年1月1日至2014年12月31日在我院行PCI和CABG患者共14230例,從臨床電子病歷數(shù)據(jù)庫中提取資料,排除基線資料、用藥情況缺失患者7707例,最終有6523例(PCI=4728,CABG=1795)患者納入統(tǒng)計(jì)學(xué)分析。結(jié)果1.在未進(jìn)行匹配的患者中,與CABG組相比,PCI組LDL-C1.8 mmol/L,LDL-C2.07 mmol/L及BP140/90mm Hg達(dá)標(biāo)率更高(P均0.01),FBG和Hb A1C達(dá)標(biāo)率在兩組之間無顯著性差異(P0.05)。傾向性評(píng)分匹配患者中LDL-C1.8 mmol/L、LDL-C2.07 mmol/L、BP140/90mm Hg、FBG及Hb A1C達(dá)標(biāo)率與未匹配患者結(jié)果一致。2.在未匹配的PCI患者中,與年齡≥60歲的患者相比,年齡60歲的患者BP140/90mm Hg達(dá)標(biāo)率顯著升高(P0.01),但LDL-C2.07mmol/L達(dá)標(biāo)率顯著降低(P0.01);在未匹配CABG患者中,與年齡≥60歲的患者相比,年齡60歲的患者FBG7 mmol/L,Hb A1c7%及BP140/90mm Hg達(dá)標(biāo)率顯著升高(P均0.01)(P0.05)。3.在未匹配的PCI患者中,與女性患者相比,男性患者LDL-C1.8 mmol/L,FBG7 mmol/L及Hb A1c7%達(dá)標(biāo)率顯著升高(P均0.01);在未匹配的CABG患者中,女性和男性性LDL-C1.8 mmol/L,LDL-C2.07 mmol/L,BP140/90mm Hg,FBG7 mmol/L及Hb A1c7%達(dá)標(biāo)率均無顯著性差異(P均0.05)。4.在傾向性評(píng)分匹配后患者中,與CABG組相比,PCI組患者出院時(shí)使用他汀、ACEI/ARB、β受體阻滯劑的比例更高(P均0.01),合用依折麥布、貝特類降脂藥物的患者比例更高(P均0.01),兩組患者中阿司匹林使用率無顯著性差異(P0.05)。5.在未匹配患者,PCI組復(fù)合終點(diǎn)事件發(fā)生率顯著高于CABG組(P0.01);在傾向性評(píng)分匹配患者,PCI和CABG患者復(fù)合終點(diǎn)事件發(fā)生率無顯著性差異(P0.05)。多變量COX回歸分析發(fā)現(xiàn)LDL-C1.8 mmol/L和HBA1C7%是影響PCI和CABG患者復(fù)合終點(diǎn)事件發(fā)生的獨(dú)立預(yù)測(cè)因子,患者LDL-C1.8mmol/L和HBA1C7%達(dá)標(biāo)與復(fù)合終點(diǎn)事件發(fā)生風(fēng)險(xiǎn)降低顯著相關(guān)。結(jié)論1.在總體和傾向性評(píng)分匹配的患者,PCI和CABG患者的血脂、血壓達(dá)標(biāo)率均存在差異,兩組患者血脂、血糖及血壓達(dá)標(biāo)率都不高;2.在PCI和CABG術(shù)后患者中,年齡60歲和年齡≥60歲患者血脂、血壓及血糖達(dá)標(biāo)率存在差異,女性和男性患者血脂、血糖達(dá)標(biāo)率存在差異;3.LDL-C1.8 mmol/L和HBA1C7%達(dá)標(biāo)與復(fù)合終點(diǎn)事件發(fā)生風(fēng)險(xiǎn)降低顯著相關(guān)。
[Abstract]:The cardiovascular and cerebrovascular diseases caused by atherosclerosis (AS) are the leading killer of human death. The formation of foam cells is one of the early signs of AS, and is also a key step for the development of AS. The main reason for the formation of foam cells is the imbalance of cholesterol inflow and outflow in macrophages. Therefore, foamer promotes foam. Intracellular cholesterol efflux inhibits the formation of foam cells and delays the occurrence and development of atherosclerotic lesions. The reverse cholesterol transport (RCT) refers to the process that HDL transfers excess cholesterol from the surrounding tissue (including atherosclerotic plaques) to the liver for the recirculation of the body or in the form of cholic acid. The flow of cholesterol in tissue cells to extracellular receptors (such as HDL), esterification and clearance of cholesterol. Recently, how to promote macrophage RCT has become a hot spot in anti atherosclerotic research. Beta 3-AR was first found in 1980, mainly in white and brown adipose tissue, and in recent years the study found its tissues in the heart, brain, lungs and liver. In recent studies, we have found that the excited Apo E-/- mouse beta 3-AR can improve blood lipid metabolism disorder, reduce TC, VLDL/LDL-C and TG, increase HDL, promote the excretion of cholesterol through bile and feces, reduce the area of atherosclerotic plaques in the thoracic aorta, and deduce that the beta 3-AR may be transported to the anti artery by promoting the reversal of cholesterol. This study used beta 3-AR agonist and antagonist to stimulate Hep G2 cells to observe the effect of supernatant on lipid and cholesterol efflux in RAW264.7 macrophage derived foam cells, explore the effect of beta 3-AR on RCT and its possible mechanism, and provide a theoretical basis for the development of a new type of anti arteriosclerosis drugs. The effect of the secretory protein on the lipid process of macrophage derived foam cells was observed by moving or inhibiting the Hep G2 cells, and the possible mechanism of the regulation of the cholesterol reverse transport (RCT) by beta 3-AR was explored. Methods the Hep G2 cells were stimulated by beta 3-AR agonist (BRL37344) and beta 3-AR antagonist (SR52390A), and the Elisa method was used to detect the supernatant. A-I, Apo A-II, Apo B and beta 3-AR content. Real-time quantitative PCR and Western blotting were used to detect the intracellular Apo A-I, Apo A-II, Apo purposes, beta, gamma and alpha content, and to induce macrophage derived foam cells by 50 micron. The staining was observed by cell morphology, the levels of intracellular total cholesterol (TC), free cholesterol (FC) and cholesteryl ester (CE), 3H labeled cholesterol to determine the cholesterol efflux rate, and the expression of ABCA1 and ABCG1 in the cells were detected by Western blot. Results 1, Elisa detection of Hep G2 cells showed that compared with the blank control group, BRL373 was compared with the control group, BRL373. The level of Apo A-I in the 44 groups was significantly higher (P0.01), and the level of Apo A-I in the group SR59230A decreased significantly (P0.01), and the Apo A-II content in the BRL37344 group was significantly lower than that in the blank control group (P0.01). Compared with the group BRL37344, the level of Apo A-I m RNA increased significantly (P0.01), and Apo A-I m RNA level in SR59230A group decreased significantly (P0.01), and there was no significant difference between the group and the blank control group. The level of beta 3-AR m RNA in group SR59230A decreased significantly (P0.01), and there was no significant difference in Apo B level in the three groups (P0.05).Apo A-I. 05) SR59230A stimulation reduced the expression level of PPAR gamma in Hep G2 cells significantly (P0.01). The expression of Apo AI protein induced by P0.05.BRL37344 stimulation could be blocked by PPAR gamma antagonist GW9662. In group SR59230A, the level of TC and CE increased significantly (P 0.05). Compared with the blank control group, the level of FC in the BRL37344 group increased significantly (P0.01), and there was no significant difference in the level of FC in the SR59230A group (P0.05).5. Compared with the blank control group, the cell supernatant significantly up-regulated the macrophage protein. There was no significant difference in the expression of ABCA1 protein in group SR59230A (P0.05), and there was no significant difference between the three groups of ABCG1 protein expression in the three groups (P0.05). Conclusion 1. excitated beta 3-AR obviously up-regulated the expression of Apo A-I protein in Hep G2 cells, and 2. excited beta 3-AR significantly up-regulated the expression of protein in the cells; 3. The up-regulated expression of Apo A-I protein in Hep G2 cells may depend on the PPAR gamma pathway, and the Hep G2 cell supernatant after 4. beta 3-AR can promote the cholesterol efflux.5. beta 3-AR excitated in the macrophage derived foam cells, and the Hep G2 cell supernatant may promote the flow of cholesterol in the foam cell by means of the pathway. Background level two preventive drugs The use of two levels of preventive drugs after percutaneous coronary intervention and coronary artery bypass surgery in patients with coronary artery bypass and coronary artery bypass surgery is rarely reported. The purpose of this study is to report on the rate of blood lipid, blood pressure, blood glucose standard and the incidence of endpoint events. The purpose of this study is to use the two level prophylaxis for patients after PCI and CABG. The analysis and comparison of the rate of blood pressure and blood glucose standard and the incidence of endpoint events were compared to investigate whether there was a difference in the control of cardiovascular risk factors in patients with PCI and CABG and the impact on the prognosis. Methods a retrospective analysis of 14230 cases of PCI and CABG patients in our hospital from January 1, 2014 to December 31, 2014, from the clinical electronic medical record database, was reviewed. The data were extracted, the baseline data were excluded, 7707 cases of drug use were missing, and 6523 patients (PCI=4728, CABG=1795) were finally included in the statistical analysis. Results 1. of the patients who were not matched, the PCI group LDL-C1.8 mmol/L, LDL-C2.07 mmol/L and BP140/ 90mm Hg were higher (P both 0.01), and two groups were in the two groups. There was no significant difference (P0.05). The rate of LDL-C1.8 mmol/L, LDL-C2.07 mmol/L, BP140/90mm Hg, FBG and Hb A1C in the tendency score matched patients were consistent with the unmatched patients in the unmatched PCI patients. Compared with those aged 60 years old, the rate of 60 years old was significantly higher. The rate of mol/L standard was significantly lower (P0.01); in patients with unmatched CABG, the rate of FBG7 mmol/L, Hb A1c7% and BP140/90mm Hg (P 0.01) was significantly higher than those aged 60 years old (P0.05) (P0.05) (P0.05). Significantly increased (P 0.01); in unmatched CABG patients, there was no significant difference between female and male sex LDL-C1.8 mmol/L, LDL-C2.07 mmol/L, BP140/90mm Hg, FBG7 mmol/L and Hb A1c7% (all 0.05). The proportion of the patients was higher (P 0.01). The proportion of the combination of ezebeb and beet lipid lowering drugs was higher (P 0.01). There was no significant difference in the use rate of aspirin in the two groups (P0.05).5. in the unmatched patients, the incidence of compound end events in the PCI group was significantly higher than that in the CABG group (P0.01); the compound end point of the patients with PCI and CABG in the tendency score matched patients, and the patients with PCI and CABG. There was no significant difference in the incidence of events (P0.05). Multivariate COX regression analysis found that LDL-C1.8 mmol/L and HBA1C7% were independent predictors of complex terminal events in PCI and CABG patients. Patients' LDL-C1.8mmol/L and HBA1C7% standards were significantly correlated with the risk reduction of complex endpoint events. Conclusion 1. matched the overall and tendency score. Patients, PCI and CABG patients with blood lipids, blood pressure standard rates are different, two groups of blood lipids, blood sugar and blood pressure standard rate is not high; 2. in PCI and CABG patients, age 60 years old and age 60 years old patients blood lipid, blood pressure and blood glucose standard rate difference, female and male patients blood lipid, blood sugar standard rate difference exists, 3.LDL-C1.8 mmol/L And HBA1C7% compliance is significantly related to the risk reduction of composite endpoint events.
【學(xué)位授予單位】:首都醫(yī)科大學(xué)
【學(xué)位級(jí)別】:博士
【學(xué)位授予年份】:2017
【分類號(hào)】:R543.5
【相似文獻(xiàn)】
相關(guān)期刊論文 前10條
1 易元杰,符水晶;美國杜邦A(yù)R全自動(dòng)生化分析儀常見報(bào)警的處理[J];現(xiàn)代檢驗(yàn)醫(yī)學(xué)雜志;2003年05期
2 李曉原,云徑平,譚潤(rùn)初,魏華江;Ar~+激光光動(dòng)力學(xué)療法對(duì)小鼠S_(180)肉瘤殺傷作用的研究[J];中華理療雜志;2000年02期
3 王康孫;魏月華;張明珩;施香荷;石海云;陳剛強(qiáng);;Ar~+激光治療視網(wǎng)膜靜脈周圍炎[J];應(yīng)用激光;1981年06期
4 楊興民;李明;;杜邦A(yù)R型全自動(dòng)生化分析儀故障維修4例[J];醫(yī)療衛(wèi)生裝備;2010年09期
5 劉連池,顧英娣;杜邦A(yù)R全自動(dòng)生化分析儀開放通道中生試劑參數(shù)的設(shè)置[J];四川省衛(wèi)生管理干部學(xué)院學(xué)報(bào);1998年04期
6 李曉原,魏華江,云徑平;Ar~+激光光動(dòng)力學(xué)療法對(duì)小鼠S_(180)肉瘤抑制作用及對(duì)腫瘤DNA含量影響的研究[J];廣東藥學(xué)院學(xué)報(bào);1998年01期
7 史有奎;馬娟;袁洲杰;孫婷;李淑蘭;;β_2-AR多態(tài)性與慢性阻塞性肺疾病的關(guān)系[J];山東醫(yī)藥;2008年13期
8 沈敬華,劉浩,高權(quán)榮,賈柄權(quán);自制抗人雄激素受體單克隆抗體檢測(cè)肝癌標(biāo)本中AR的表達(dá)[J];內(nèi)蒙古醫(yī)學(xué)院學(xué)報(bào);2003年01期
9 張俊峰;葛恒;郭炳詩;邵琴;王長(zhǎng)謙;;細(xì)胞外基質(zhì)金屬蛋白酶誘導(dǎo)因子在巨噬和泡沫細(xì)胞中的表達(dá)[J];上海交通大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2006年03期
10 徐元根;;“泡沫”細(xì)胞[J];國外醫(yī)學(xué)情報(bào);1982年14期
相關(guān)會(huì)議論文 前10條
1 馬潔;;船舶縱搖運(yùn)動(dòng)預(yù)報(bào)AR法與多層遞階方法比較研究[A];2009年中國智能自動(dòng)化會(huì)議論文集(第二分冊(cè))[C];2009年
2 邱華寧;吳河勇;馮子輝;施和生;云建兵;梅廉夫;方偉;霍秋立;李景坤;王雪;朱俊章;;油氣成藏~(40)Ar/~(39)Ar年代學(xué)研究重要突破[A];中國礦物巖石地球化學(xué)學(xué)會(huì)第13屆學(xué)術(shù)年會(huì)論文集[C];2011年
3 魯艷軍;田俊;狄勇;孫自鏞;;富含甘油三酯的泡沫細(xì)胞的雙向熒光差異凝膠電泳[A];中華醫(yī)學(xué)會(huì)第九次全國檢驗(yàn)醫(yī)學(xué)學(xué)術(shù)會(huì)議暨中國醫(yī)院協(xié)會(huì)臨床檢驗(yàn)管理專業(yè)委員會(huì)第六屆全國臨床檢驗(yàn)實(shí)驗(yàn)室管理學(xué)術(shù)會(huì)議論文匯編[C];2011年
4 張曉暉;李鐵勝;王輝;蒲志平;;內(nèi)蒙赤峰婁子店—大城子韌性剪切帶的~(40)Ar-~(39)Ar年齡及其構(gòu)造意義[A];中國科學(xué)院地質(zhì)與地球物理研究所2002學(xué)術(shù)論文摘要匯編[C];2002年
5 李偉;卞直上;龔建;向永春;王紅俠;何美英;段榮良;張偉;;移動(dòng)式~(37)Ar快速測(cè)量原型系統(tǒng)研制[A];中國工程物理研究院科技年報(bào)(2005)[C];2005年
6 魯艷軍;田俊;狄勇;宗義強(qiáng);王淳本;屈伸;;VLDL誘導(dǎo)THP-1形成泡沫細(xì)胞的蛋白質(zhì)組學(xué)研究[A];湖北省暨武漢市生物化學(xué)與分子生物學(xué)學(xué)會(huì)第八屆第十七次學(xué)術(shù)年會(huì)論文匯編[C];2007年
7 孟華;;基于PCI總線的PC機(jī)再入遙測(cè)站平臺(tái)設(shè)計(jì)[A];中國工程物理研究院科技年報(bào)(2003)[C];2003年
8 陳燕;劉志虹;曾彩虹;黎磊石;;腎小球疾病患者腎間質(zhì)泡沫細(xì)胞及其臨床意義[A];中華醫(yī)學(xué)會(huì)腎臟病學(xué)分會(huì)2006年學(xué)術(shù)年會(huì)論文集[C];2006年
9 王偉鈞;唐小我;楊晉浩;;滿足AR(1)需求過程的零售商庫存決策和牛鞭效應(yīng)[A];第四屆中國智能計(jì)算大會(huì)論文集[C];2010年
10 施鴻毓;張紅旗;孫愛軍;姚康;黃榕,
本文編號(hào):2019382
本文鏈接:http://sikaile.net/yixuelunwen/xxg/2019382.html