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1.
目的检测白细胞介素-4(IL-4)受体α链(IL-4Rα)I50V和Q576R基因多态性与呼吸道合胞病毒(RSV)毛细支气管炎的相关性。方法采用聚合酶链-限制性片段长度多态法检测130例RSV毛细支气管炎患儿和108例健康儿童IL-4Rα/I50V、Q576R基因多态性,应用化学发光法和酶联免疫吸附法检测血清总IgE和鼻咽分泌物(NPS)IL-4R水平。结果病例组II、IV和VV基因型频率为24.6%、51.5%和23.9%,对照组为27.8%、40.7%和31.5%,差异无统计学意义(χ2=2.960,P0.05);病例组I、V等位基因频率为50.4%、49.6%,对照组为48.1%、51.9%,差异无统计学意义(χ2=0.236,P0.05),II基因型NPS中IL-4R高于IV和VV基因型(Z=2.031,2.034,P0.05)。病例组QQ和QR基因型频率为72.3%、27.7%,对照组为64.8%、35.2%,差异无统计学意义(χ2=0.521,P0.05);病例组Q、R等位基因频率为86.2%、13.8%,对照组为82.4%、17.6%,差异无统计学意义(χ2=1.261,P0.05),R等位基因携带者NPSIL-4R高于Q等位基因携带者(Z=2.205,P0.05)。两个位点基因型间血清总IgE差异无统计学意义(F=1.021,t=0.452,P0.05);基因型频率与病情间亦无关联(χ2=0.322,1.393,P0.05)。结论 IL-4Rα/50II基因型及576R等位基因携带者与RSV毛细支气管炎NPSIL-4R水平增高相关。  相似文献   

2.
目的 探讨血小板活化因子乙酰水解酶( PAF-AH)基因Ala379Val、Val279Phe位点多态性与脓毒症易感性及预后的关系.方法 采用PCR-RFLP技术,分析66例不同程度的脓毒症患者及68名健康对照者PAF-AH基因Ala379Val、Val279Phe位点的多态性,对含有等位基因多态性的片段进行DNA测序分析,SPSS13.0软件进行统计学分析.结果 全部样本经PCR-RFLP分析后,在PAF-AH基因Ala379Val位点3种基因型中,脓毒症组66例中仅1例纯合子Val/Val型,19例杂合子Val/Ala型,46例纯合子Ala/Ala型;对照组68例中2例Val/Val型,22例Val/Ala型,44例Ala/Ala型.Ala379Val基因型及等位基因频率分布在脓毒症组和对照组之间、存活组和死亡组之间尚无统计学意义(P>0.05).在PAF-AH基因Val279Phe位点3种基因型中,脓毒症组66例中全部为纯合子Val/Val型,对照组68例中仅1例纯合子Phe/Phe型,其余全部为纯合子Val/Val型,未发现杂合子Val/Phe型.Val279Phe基因型及等位基因频率分布在对照组和脓毒症组之间、存活组和死亡组之间尚无统计学意义(P>0.05).结论 PAF-AH基因Ala379Val、Val279Phe位点多态性存在蛋白质一级结构差异的较大可能,与脓毒症易感性、预后可能不相关.  相似文献   

3.
神经源分化因子基因多态性与2型糖尿病的关联性研究   总被引:1,自引:0,他引:1  
目的 探讨神经源分化因子 (neurogenic differentiation factor 1,Neuro D)基因多态性与 2型糖尿病发生的关联性。方法 运用错配聚合酶链反应 -限制性片段长度多态性方法检测了中国湖北地区汉族 32 4例 2型糖尿病 (其中以发病年龄 40岁为界 ,分为早发及晚发两组 )及 12 4名正常对照者 ,Neuro D基因第 45位密码子碱基变异 (GCC→ ACC)。结果  Neuro D基因在所测人群中未发现有纯合变异者。在早发 2型糖尿病组 ,其 AT基因型频率为 2 6 .8% ,与正常对照组 (10 .5 % )及晚发 2型糖尿病组 (11.6 % )比较 ,差异有显著性 (分别为χ2 =7.85 ,P=0 .0 0 5 ;χ2 =8.81,P=0 .0 0 3) ;Thr45等位基因频率在早发 2型糖尿病组及正常对照组、晚发 2型糖尿病组分别为 13.4%、5 .2 %和 5 .8% ,差异亦有显著性 (χ2 =7.15 ,P=0 .0 0 8;χ2 =8.13,P=0 .0 0 4) ;晚发 2型糖尿病组与正常对照组比较 ,Ala45 Thr基因型频率 (11.6 % vs10 .5 % ,P>0 .0 5 )及等位基因频率 (5 .8% vs 5 .2 % ,P>0 .0 5 )差异不明显 ,Thr45等位基因与早发 2型糖尿病发生相关 (OR=2 .5 2 ,95 % CI:1.42~ 4.49) ;基因型为 AT型的 2型糖尿病患者其空腹血浆 C肽水平较 AA型患者低 ,差异有显著性 (P<0 .0 5 )。结论  Neuro D基因多态性与早发 2型糖尿  相似文献   

4.
糖尿病视网膜病变患者检测糖化血红蛋白的临床意义   总被引:2,自引:0,他引:2  
目的探讨糖尿病视网膜病变 (DR)患者检测糖化血红蛋白 (HbA1c)的临床意义。方法对154例2型糖尿病患者DR情况和HbA1c水平进行检测。并对71例、病程5~10年的糖尿病患者正常眼底 (NDR)或单纯型糖尿病视网膜病变 (BDR)患者进行1年的随访 ,检测DR进展情况和HbA1c水平。结果DR组HbA1c高于NDR组。增殖型糖尿病视网膜病变 (PDR)组HbA1c高于BDR组。随访1年 ,视网膜病变进展组(A组)平均HbA1c高于视网膜病变稳定组(B组),差异具有统计学意义 (P<0.01)。结论DR的程度和进展与HbA1c增高有关  相似文献   

5.
目的 研究过氧化物体增殖活化受体γ2(peroxisome proliferator activated receptorγ2,PPARγ2)基因Pro12Ala和C1431T多态性及其单倍型与汉族人2型糖尿病、肥胖的关系.方法 应用聚合酶链反应-限制性片段长度多态性的方法,对207例2型糖尿病患者和101名非糖尿病对照者进行PPARγ2基因Pro12Ala和C1431T多态性研究.结果 (1)在非糖尿病对照人群中Aal 12等位基因频率是0.064,T1431等位基因频率是0.252.单倍型分析显示Pro12Ala和C1431T两个位点连锁不平衡(D'=0.63,r2=0.074),组成了3种常见单倍型Pro-C、Pro-T和Ala-T.(2)Pro12Ala和C1431T多态性分布及其单倍型分布频率在2型糖尿病组与对照组组间差异均无统计学意义(P>0.05).(3)Pro12Ala变异与糖尿病患者的血压、血脂相关,地等位基因降低非肥胖糖尿病患者的舒张压(P<0.05),而对肥胖糖尿病患者的血脂水平无保护作用(P<0.05);C1431T多态性与糖尿病患者的超重和肥胖相关,超重和肥胖的糖尿病者T等位基因频率相对较高(P<0.05).结论 Pro12Ala和C1431T多态性可能在汉族人糖尿病发病中不是起主要作用;C1431T多态性与糖尿病患者的超重和肥胖相关.  相似文献   

6.
闫宇梅 《医学信息》2018,(17):89-91
目的 探讨CysC与Hcy与2型糖尿病视网膜病变的相关性。方法 选取我院2017年1月~12月收治的2型糖尿病患者160例,根据眼底照相结果分为糖尿病视网膜病变组(DR组)和糖尿病无视网膜病变组(NDR组),每组80例,同时选取健康受试者80例作为对照组。观察各组患者血糖、血脂、血清CysC及Hcy水平。结果 ①DR组和NDR组SBP、DBP、FBG、2hBG、TG、TC、LDL-C、BUN、SCr、HbA1C、CysC和Hcy水平均高于对照组,差异具有统计学意义(P<0.05);DR组和NDR组HDL-C水平低于对照组,差异具有统计学意义(P<0.05);DR组SBP、TG、SCr、CysC和Hcy水平高于NDR组,差异具有统计学意义(P<0.05)。②CysC与病程、TG、SCr、Hcy呈正相关(r=0.428、0.490、0.479、0.215,P<0.05),与BMI、SBP、LDL-C、FBG无明显相关性。③Logistic多元回归分析显示:TG、SBP、CysC和Hcy为影响2型糖尿病视网膜病变发生的危险因素。结论 高CysC及Hcy水平是发生糖尿病视网膜病变的危险因素,CysC联合Hcy检测对2型糖尿病视网病变的诊治有一定指导意义。  相似文献   

7.
目的 探讨甘露糖结合凝集素2(mannosC-binding lectin 2,MBL2)基因rsl800450、rsl800451、rsll003125位点及蛋白激酶C-β1(protein kinase C-β1,PRKC-β1)基因rs3700106、rs2575390此5个位点的多态性及其单倍型与中国北方汉族人群2型糖尿病(type 2 diabetes mellitus,T2DM)大血管并发症(macrovascular complications,MA)的关系.方法 收集318例北方汉族了2DM患者和448名血糖正常健康对照,应用多重SNaPshot技术对病例组和无对照组的上述5个位点多态性进行检测,应用Haploview软件对5个位点进行连锁不平衡分析和单倍型分析,采用相加模型研究基因变异与环境之间交互作用对MA的影响.结果 与血糖正常的对照组相比,MA患者中心血管病变组和周围血管病变组在rs11003125多态位点上基因型频率差异均有统计学意义,户值分别为0.024和0.004,等位基因频率差异也均有统计学意义,P值分别为0.014和0.001;与无MA的72DM患者相比,周围血管病变组在rs11003125位点上的等位基因频率差异有统计学意义(P=0.031);其它位点基因型和等位基因频率在3种大血管病变组与对照组和无MA组间的分布差异均无统计学意义.单倍型分析结果显示无论与对照组还是无MA组相比,同时携带rs1800450位点G等位基因和rs11003125位点C等位基因的研究对象患MA的风险明显增高.结论 MBL2基因启动子rs11003125多态与T2DM患者MA可能相关,携带rs1800450位点G等位基因以及rs11003125位点C等位基因可能是中国北方汉族T2DM患者发生MA的危险因素.Rs11003125位点(GC+CC)变异与高血压、糖尿病肾病、糖尿病神经病变及视网膜病变在致MA的过程中可能存在正相加交互作用.  相似文献   

8.
目的 探讨汉族人群肝脂酶(hepatic lipase,HL)基因启动子-250G/A多态性与2型糖尿病(type 2 diabetes mellitus,T2DM)合并冠心病(coronary heart disease,CHD)的相关性.方法 采用聚合酶链反应-限制性片段长度多态性方法(polymerase chain reaction-restricted fragment length polymorphism,PCR-RFLP)检测364例T2DM+CHD组、357例T2DM组患者和356名健康对照者HL基因启动子-250G/A多态性,并分析其对脂类的影响.结果 T2DM组与对照组HL基因启动子-250G/A多态性基因型和等位基因频率差异无统计学意义(P>0.05);T2DM+CHD组GA+AA基因型频率低于对照组(0.431 vs 0.618,P=0.031);等位基因频率差异无统计学意义(P>0.05).调整混杂因素后,Spearman相关及线性回归分析,糖尿病患者(T2DM组和T2DM+CHD组),A等位基因与高密度脂蛋白胆固醇、载脂蛋白A1呈正相关;Logistic回归分析显示,A等位基因是冠心病发生的一个危险因素.结论 HL基因启动子-250G/A多态性与2型糖尿病合并冠心病的发生有关,并影响脂类代谢.  相似文献   

9.
目的 :研究FVal34Leu基因多态性在汉族人群中的分布情况 ,并探讨其与冠心病及心肌梗死的关系。方法 :应用聚合酶链反应 -单链构像多态性技术检测 398例汉族人 (冠心病组 195例 ,对照组 2 0 3例 )的F基因Val34Leu突变基因型。结果 :Val/Val基因型和Val/Leu基因型频率分别为 95 2 %和 4 8% ,未发现Leu/Leu基因型 ,Leu等位基因频率为 2 4 %。冠心病组和对照组间基因型和等位基因频率无显著差异 (P >0 0 5 )。非心肌梗死组Val/Leu基因型和Leu等位基因分布频率显著高于心肌梗死组 (P <0 0 5 )。结论 :中国汉族人群中存在FVal34Leu基因多态性  相似文献   

10.
目的 研究2型糖尿病(type 2 diabetes mellitus,T2DM)及其肾病(diabetic nephropathy,DN)发生、发展与血管生成素2(angiopoietin-2,Ang-2)基因多态性的关联性.方法 应用等位基因特异聚合酶链反应检验无亲缘关系汉族人群的2型糖尿病及其肾病患者221例、正常对照104名Ang-2基因单核苷酸多态性(single nucleotide polymorphism,SNP)759T/G、1078A/G、1233A/G在病例组中的频率,并用尿白蛋白排泄率、炎症标志物单核细胞趋化蛋白浓度变化探讨上述SNP与T2DM、DN发生发展的关联.结果 (1) Ang-2 759 T/G、1078 A/G基因型频率和等位基因频率在各组中的差异无统计学意义,而1233 A/G基因型频率和等位基因频率的差异有统计学意义(P<0.05);(2)在校正年龄和性别等因素后,1233A/GSNP G等位基因患T2DM和DN的风险分别是A等位基因的2.265倍(95% CI:1.223~1.402,P=0.031)和1.789倍(95% CI:0.889~1.021,P=0.012);(3) Ang-2 1233A/G G等位基因与DN发生相关(r=1.321,OR=1.427,95% CI:2.324~4.177,P=0.034).结论 Ang-2 1233A/G SNP与2型糖尿病的发生有关;AG+ GG基因型和等位基因G可能是DN发生、发展的风险因素.  相似文献   

11.
OBJECTIVE: To investigate the association of the polymorphism in manganese superoxide dismutase (Mn-SOD) gene in Chinese type 2 diabetic patients with diabetic retinopathy. METHODS: The Ala(-9)Val polymorphism of the Mn-SOD gene was determined by polymerase chain reaction and direct sequencing in 198 normal control subjects and 264 patients with type 2 diabetes mellitus, among them there were 139 non-diabetic retinopathy (NDR) subjects and 125 subjects with diabetic retinopathy (DR). RESULTS: There was no statistic difference in the frequencies of VV genotype and V allele between the type 2 diabetic group and the control group. However, the frequencies of VV genotype and V allele were significantly higher in the DR group than that in the NDR group (chi-square (2)=5.015, P=0.025?chi-square (2)=10.253, P=0.001),but there was no statistic difference in the NDR group compared with the control group (P > 0.05). The presence of V allele was shown to be associated with diabetic retinopathy (OR=1.96, 95%CI: 1.29-2.97). Furthermore, the subjects carrying the VV genotype had lower serum Mn-SOD level (P=0.025) and had a tendency of higher total serum SOD activity, but this tendency had no statistic significance. CONCLUSION: The Ala(-9)Val polymorphism in the Mn-SOD gene may not be related to the etiology of type 2 diabetes, but it seems to contribute to the development of diabetic retinopathy in Chinese type 2 diabetic patients.  相似文献   

12.
 We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients. Val(16)Ala genotyping of Mn-SOD was done by polymerase chain reaction-restriction fragment length polymorphism with a restriction enzyme (Bsaw I) in 478 Japanese type 2 diabetic patients and 261 nondiabetic Japanese healthy subjects. The genotype distribution of diabetic and nondiabetic subjects was then compared, and the association of genotype with diabetic nephropathy was evaluated in the diabetic patients. The allele frequency and genotype of the diabetic patients were not different from those of the healthy nondiabetic subjects. The VV type showed a significantly higher frequency in the diabetic patients with nephropathy than did the AA or VA type [VV type: normoalbuminuria 70.8%, microalbuminuria 84.8% (P = 0.0057), macroalbuminuria 84.1% (P = 0.0128)]. Furthermore, logistic regression analysis showed that this polymorphism is associated with diabetic nephropathy independently (odds ratio = 0.461925, P = 0.03). Accordingly, the Val(16)Ala polymorphism of Mn-SOD may be unrelated to the etiology of type 2 diabetes, but it seems to be associated with diabetic nephropathy in Japanese type 2 diabetic patients. Received: August 5, 2002 / Accepted: December 3, 2002 Correspondence to:Y. Tanaka  相似文献   

13.
Substantial data indicate that oxidative stress is involved in the development of diabetic retinopathy. Two candidate genes that affect the oxidative stress are manganese mitochondrial superoxide dismutase (Mn-SOD) and endothelial nitric oxide synthase (eNOS). The aim of the present study was to examine the role of the V16A polymorphism of the Mn-SOD gene and the 4a/b polymorphism of the eNOS gene in the development of diabetic retinopathy in Caucasians with type 2 diabetes. In this cross sectional case-control study 426 unrelated Slovene subjects (Caucasians) with type 2 diabetes mellitus were enrolled: 283 patients with diabetic retinopathy and the control group of 143 subjects with type 2 diabetes of duration of more than 10 years who had no clinical signs of diabetic retinopathy. A significantly higher frequency of the VV genotype of the V16A polymorphism of the Mn-SOD was found in patients with diabetic retinopathy compared to those without diabetic retinopathy (OR=2.1, 95% whereas the 4a/b polymorphism of the eNOS gene failed to yield an association with diabetic retinopathy. We may conclude that the VV genotype of the V16A polymorphism of the Mn-SOD gene was associated with diabetic retinopathy in Caucasians with type 2 diabetes, therefore it might be used as a genetic marker of diabetic retinopathy in Caucasians.  相似文献   

14.
 目的:色素上皮衍生因子(PEDF)是影响糖尿病视网膜病变(DR)发生发展的重要因子,本研究观察2型糖尿病视网膜病变患者外周血单个核细胞(PBMCs)中PEDF、磷酸化NF-κB p65及TNF-α的表达,探讨DR的发病机制。方法:选取2011年10月~2013年4月在我院内分泌科住院确诊为2型糖尿病的患者(DM组)108例,并根据眼底造影结果将患者分为无糖尿病视网膜病变组(NDR组)52例和糖尿病视网膜病变组(DR组)56例,同期糖耐量实验正常者52例作为对照组(NC组)。密度梯度离心法收集患者 PBMCs,提取总蛋白,Western blotting检测3组患者PBMCs中PEDF、磷酸化NF-κB p65和TNF-α蛋白表达水平,ELISA测定血浆PEDF与TNF-α水平,收集患者体检指标并测量患者生化指标。结果:Western blotting检测结果显示NDR组和DR组PEDF、磷酸化NF-κB p65和TNF-α蛋白水平明显高于NC组(P<0.05);DR组TNF-α蛋白水平明显高于NDR组(P<0.05),DR组PEDF及磷酸化NF-κB p65蛋白水平略高于NDR组,差异无统计学意义(P>0.05);NDR组和DR组血浆PEDF与TNF-α水平均明显高于NC组(P<0.05),DR组明显高于NDR组(P<0.05)。在糖尿病组,血浆PEDF水平与TNF-α及血尿酸水平呈正相关(r=0.39,r=0.25,P<0.05)。结论:本研究首次证实PBMCs中可表达PEDF;2型糖尿病患者PBMCs中PEDF表达水平增加,TNF-α及血浆PEDF的表达水平上调,PEDF可能通过与炎症因子TNF-α相互作用影响DR发生发展。  相似文献   

15.
高同型半胱氨酸血症对2型糖尿病视网膜病变的影响   总被引:1,自引:0,他引:1  
目的:探讨高同型半胱氨酸( HHcy)对2型糖尿病视网膜病变(DR)发生发展的影响。方法:检测152例2型糖尿病(T2DM)患者,包括DR组和非视网膜病变(NDR)组各76例以及50例同期健康体检者(对照组)血浆总Hcy(t Hcy)浓度、空腹血糖(FBG)、空腹胰岛素(FI NS)、糖化血红蛋白( HbA1c)、血脂等,并对上述指标及临床资料进行回顾性分析。结果:DR组血浆t Hcy水平高于NDR组及对照组(P<0 .01) ;DR组中增值型视网膜病变(PDR)亚组t Hcy水平高于背景型视网膜病变(BDR)亚组(P<0 .05) ;Logistic回归分析示,DR的发生与病程、HbA1c、t Hcy和胆固醇有关,血浆t Hcy水平是DR的独立危险因素。结论:HHcy血症是T2DM患者DR发生发展的重要的危险因子之一。  相似文献   

16.
目的:研究亚甲基四氢叶酸还原酶(methylenetetrahydrofolate reductase,MTHFR)基因多态性及血浆同型半胱氨酸水平与2型糖尿病视网膜病的关系。方法:应用聚合酶链反应-限制性内切酶片段长度多态性技术检测208例2型糖尿病患者(其中110例伴视网膜病)及57名正常对照的MTHFR C677T基因型,采用高效液相色谱法测定血浆同型半胱氨酸水平。结果:糖尿病视网膜病组MTHFR基因TT纯合基因型、CT杂合基因型及T等位基因频率(分别为28.18%、41.82%、49.09%)均明显高于糖尿病不伴视网膜病组(分别为18.37%、29.59%、33.16%)及正常对照组(分别为17.54%、28.07%、31.58%),基因型和等位基因频率分布差异均有显著性(P<0.01),而MTHFR基因多态性在糖尿病不伴视网膜病组与正常对照组之间差异无显著性(P>0.05),T等位基因与糖尿病视网膜病的发生密切相关(OR=1.94,95%CI;1.31-2.88)。糖尿病视网膜病组、糖尿病不伴视网膜病组及正常对照组中,MTHFR基因有C677T突变者血浆同型半胱氨酸水平均显著高于无基因突变者。结论:MTHFR基因C677T位碱基突变致血浆同型半胱氨酸水平升高可能是糖尿病视网膜病发病的重要遗传因素。  相似文献   

17.
Catalase is a central antioxidant enzyme constituting the primary defense against oxidative stress. In this study, we investigated whether the functional -262C/T polymorphism in the promoter of catalase gene is associated with the presence of diabetic retinopathy (DR), diabetic nephropathy (DN) and ischemic heart disease (IHD) in 520 Caucasian-Brazilians with type 2 diabetes. The -262C/T polymorphism was also examined in 100 Caucasian blood donors. Patients underwent a clinical and laboratory evaluation consisting of a questionnaire, physical examination, assessment of diabetic complications and laboratory tests. Genotype analysis was performed using the polymerase chain reaction followed by digestion with restriction enzyme. The genotype and allele frequencies of the -262C/T polymorphism in patients with type 2 diabetes were very similar to those of blood donors (T allele frequency=0.20 and 0.18, respectively). Likewise, there were no differences in either genotype or allele frequencies between type 2 diabetic patients with or without DR, DN or IHD. Thus, our results do not support the hypothesis that the -262C/T polymorphism is related to the development of DR, DN or IHD in patients with type 2 diabetes. Further studies are necessary to elucidate the role of catalase gene polymorphisms in the pathogenesis of diabetic complications.  相似文献   

18.
19.
Melatonin is a powerful antioxidant. Decreased melatonin excretion has been reported to be associated with several oxidative stress-related diseases. The urinary metabolite of melatonin, 6-sulfatoxymelatonin (aMT6s), has proved to be a very reliable index of melatonin production. The present study aims to evaluate the level of urinary aMT6s in patients with type 2 diabetes mellitus and diabetic retinopathy. Urine samples were collected from 10 patients with diabetes and no diabetic retinopathy (NDR), 19 patients with nonproliferative diabetic retinopathy (NPDR), 38 patients with proliferative diabetic retinopathy (PDR), and 16 subjects without diabetes mellitus, who served as controls. The level of aMT6s in specimens was assayed by a commercial aMT6s ELISA kit, creatinine levels were also measured for each sample to get urinary aMT6s/creatinine ratio. Creatinine-adjusted urinary aMT6s values were compared among four groups. The urinary aMT6s (mean ± SD) levels were 9.95 ± 2.42, 9.90 ± 2.28, 8.40 ± 1.84 and 5.58 ± 1.33 ng/mg creatinine in the controls and in patients with NDR, NPDR, or PDR, respectively. The urinary aMT6s level of the PDR group was significantly lower than that of the control, NDR and DR groups. No significant difference was found among the control, NDR and DR groups. After adjustment for various factors (age, smoking, cancer, and coronary heart disease) that may influence the aMT6s level, the odds-ratio of urinary aMT6s comparing PDR patients to controls was 0.246 (95% confidence interval = 0.108-0.558, P = 0.001). Therefore, the urinary aMT6s level is significantly decreased in diabetic patients with PDR but not in diabetic patients without PDR, which indicates that decreased urinary aMT6s level may be associated with the pathogenesis of PDR.  相似文献   

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