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1.
目的:探讨体外受精-胚胎移植(IVF-ET)过程中基础卵泡刺激素(bFSH)水平及年龄与卵巢反应性及IVF治疗结局的相关性.方法:对2008年6月至2010年6月在我生殖中心接受IVF-ET治疗的402例不孕症患者新鲜周期结局进行回顾性分析,根据不同bFSH水平组合不同年龄分组患者:低龄高bFSH组(226例)(年龄<38岁且bFSH≥12 IU/L)与高龄低bFSH组(182例)(年龄≥38岁且bFSH<12 IU/L),比较两组卵巢反应性和IVF-ET结局的差异.结果:低bFSH组患者获卵数目明显多于高bFSH组(P=0.016),但两组Gn用药天数及剂量的差异无统计学意义(P>0.05).两组治疗周期取消率、周期获卵率、受精率、卵裂率及优胚率等方面的差异无显著性意义(P>0.05),而低龄高bFSH组患者在胚胎种植率(P=0.00)、临床妊娠率(P=0.002)及流产率(P=0.030)三方面的结局明显优势于高龄低bFSH组.结论:基础FSH是评估卵巢反应性的良好指标,但不能较好地预测妊娠结局;年龄是预测IVF治疗结局的较独立指标,与最终的临床妊娠、流产结局密切相关.  相似文献   

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目的探讨男性精液参数与体外受精(IVF)-胚胎移植妊娠结局的相关性。方法收集2013年1月至2014年12月东莞康华医院生殖中心第1周期长方案IVF-胚胎移植的371个周期,分析不同妊娠结局中男性精液参数的差异。结果临床妊娠组和未妊娠组精子密度、活率、活力和精子正常形态百分比差异均无统计学意义(P0.05)。结论精液参数对IVF临床妊娠结局的预测价值比较有限。  相似文献   

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目的探讨子宫内膜异位症患者体外受精-胚胎移植前应用低剂量促性腺激素释放激素激动剂2个周期对治疗结局的影响。方法子宫内膜异位症患者为A组(25周期)体外受精-胚胎移植前每28d应用1.80mg促性腺激素释放激素激动剂,共2个周期,因输卵管因素而行GnRH-a标准长方案患者为B组(90周期),比较两组促排前E2、LH的水平,HCG日E2、LH水平、p值,出现LH峰的比率,促性腺激素用量、促排天数、获卵数、受精率、优质胚胎率、种植率、临床妊娠率。结果1.80mg促性腺激素释放激素激动剂预处理组无LH峰的出现,也未出现降调过度,促性腺激素用量显著高于常规GnRH-a长方案组,而促排天数、获卵数、受精率、优质胚胎率、种植率、临床妊娠率无显著性差异。结论与传统方法相比,应用1.80mgGnRH-a预处理子宫内膜异位症患者2个月,不影响体外受精-胚胎移植的临床妊娠率,同时缩短了治疗时间,降低了患者的费用。  相似文献   

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目的探讨体质指数(BMI)对体外受精-胚胎移植(IVF-ET)或卵胞浆内单精子显微注射(ICSI)治疗过程及结局的影响。方法回顾性分析本中心2009年1月至2010年9月共1 201例应用长方案IVF/ICSI治疗的患者,按照世界卫生组织推荐的分组标准分为三组。其中低体质量组(A组)100例,正常体质量组(B组)973例,超重和肥胖组(C组)128例。比较各组超促排卵过程中各项指标及妊娠结局。结果 C组平均促性腺激素(Gn)用量较A、B两组明显增多(P<0.05),注射人绒毛膜促性腺激素(hCG)日血清雌二醇(E2)值较A、B两组明显减少(P<0.05)。C组与B组比较,受精率(81.0%vs.83.7%)和优胚率(47.08%vs.53.8%)明显降低(P均<0.017);A组的种植率(35.1%)低于B组(45.3%)(P<0.017)。三组在获卵数、临床妊娠率、自然流产率、异位妊娠率、周期取消率方面比较,差异均无统计学意义(P>0.05)。结论随着患者BMI的增加,Gn用量明显增多。本研究尚未发现BMI对IVF/ICSI妊娠结局有显著影响。  相似文献   

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目的:分析体重指数(BMI)对多囊卵巢综合征(PCOS)患者体外受精-胚胎移植(IVF-ET)妊娠结局的影响。方法:选取2015年1月~2017年3月于洛阳市妇女儿童保健中心行IVF-ET的PCOS患者220例,以BMI为依据分为肥胖组125例(BMI≥24.0 kg/m~2)和正常组95例(18.5 kg/m~2≤BMI24.0 kg/m~2)。两组均进行IVF-ET治疗,比较两组促排天数、Gn用量、获卵数、优质胚胎数及妊娠结局。结果:肥胖组促排天数、Gn剂量高于正常组,优质胚胎数、获卵数低于正常组(P0.05);肥胖组胚胎着床率低于正常组,早期流产率高于正常组(P0.05);肥胖组妊娠率低于正常组,但差异无统计学意义(P0.05)。结论:BMI降低有助于减少促排时间及Gn用量,增加获卵数与优质胚胎数,提高胚胎着床率,降低早期流产率,改善PCOS患者IVF-ET妊娠结局。  相似文献   

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目的探讨血清及卵泡液中25-羟维生素D[25(OH)D]与体外受精-胚胎移植(IVF-ET)妊娠结局的关系。 方法选取2017年7月至2018年7月于山西医科大学第一医院生殖中心首次接受IVF-ET助孕治疗的67例不孕患者,按照妊娠结局分为妊娠组和未妊娠组。采用t检验或秩和检验比较2组间的实验室检查数据以及血清及卵泡液中25(OH)D的差异,差异具有统计学意义的变量进行Logistic多因素回归分析;采用Pearson相关分析法分析血清25(OH)D水平与卵泡液25(OH)D水平的相关性,采用Spearman相关分析法分析血清25(OH)D水平与三酰甘油、促甲状腺素、受精率的相关性。 结果所有患者平均血清25(OH)D水平为26.27 μg/L。(1)妊娠组与未妊娠组促甲状腺素[2.34(1.80~3.20)mIU/ml vs 2.93(2.28~4.53)mIU/ml]、三酰甘油[0.93(0.73~1.22)mmol/L vs 1.14(0.87~1.56)mmol/L]、Gn起始剂量[225.0(150.0~300.0)IU/L vs 262.5(225.0~300.0)IU/L]比较均低,差异均具有统计学意义(Z=-2.237、-2.138、-2.107,P=0.020、0.032、0.035);妊娠组与未妊娠组的受精率[85.7%(78.3%~94.4%)vs 76.3%(63.5%~92.5%)]、血清及卵泡液中25(OH)D[血清:(37.08±13.39)mmol/L vs(28.90±12.53)mmol/L;卵泡液:(31.18±13.10)mmol/L vs (21.92±9.24)mmol/L]比较均高,差异均具有统计学意义(Z=-2.178,P=0.029;t=2.579、3.282,P=0.012、0.020)。(2)IVF-ET患者血清25(OH)D与卵泡液25(OH)D水平呈正相关(r=0.836,P<0.01),与三酰甘油水平呈负相关(r=-0.286,P=0.019),与促甲状腺素水平无相关性(r=-0.007,P=0.958),与受精率呈正相关性(r=0.43,P<0.01)。(3)Logistic回归分析临床妊娠结局的影响因素结果显示血清25(OH)D、卵泡液25(OH)D、三酰甘油、促甲状腺素、Gn起始剂量、受精率在去除混杂因素后,对IVF-ET患者妊娠结局无明显影响(P均>0.05),将血清与卵泡液25(OH)D联合之后再进行回归分析发现在去除混杂因素后,对IVF-ET患者妊娠结局也无明显影响(比值比=1.001,P=0.058)。 结论不孕症患者普遍存在维生素D缺乏,但维生素D和IVF-ET临床妊娠结局无明显相关性。  相似文献   

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目的探讨定坤丹预处理对卵巢低反应(POR)患者卵巢储备功能及体外受精-胚胎移植(IVF-ET)结局的影响。方法选取2018年1月至2019年10月在本院妇产科生殖中心接受IVF-ET治疗的220例POR患者为研究对象,随机将其分为研究组(行定坤丹预处理)和对照组(未行预处理),各110例。比较两组预处理前、后的卵巢储备功能指标及IVF-ET周期治疗指标。结果研究组预处理后FSH水平低于预处理前及对照组,AMH水平高于预处理前及对照组,AFC多于预处理前及对照组,差异具有统计学意义(P<0.05)。研究组获卵数多于对照组,受精率IVF-ET周期取消率低于对照组,高于对照组,差异具有统计学意义(P<0.05);两组Gn总量、优质胚胎率、胚胎种植率、临床妊娠率比较,差异无统计学意义(P>0.05)。结论采用定坤丹预处理可改善POR患者卵巢储备功能,降低IVF-ET周期取消率,为临床结局改善提供新思路。  相似文献   

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[目的]探讨病人行体外受精-胚胎移植(IVF-ET)的病因及各因素对妊娠分娩结局的影响。[方法]回顾性分析216例IVF-ET术后住院分娩的病人,根据不孕的主要因素分为4组,输卵管卵巢因素组、子宫内膜因素组、男方因素组和不明原因组,比较4组的自然流产率、异位妊娠率、早产率,总结并分析妊娠产科并发症及分娩方式。[结果]输卵管卵巢因素组异位妊娠率高(7.84%),子宫内膜组自然流产率高(20.75%),与其余各组比较差异均有统计学意义(P0.05)。产妇妊娠并发症以妊娠糖尿病、妊娠高血压居多,剖宫产率82.87%,但无手术指证的产妇拒绝试产要求剖宫产的比率占到36.87%。[结论]IVF-ET术后孕妇因产科并发症及社会因素引起的剖宫产率高,在分析IVF-ET结局时应注意各病因对其的影响,针对病因预防性治疗,以提高IVF-ET的成功率,改善妊娠结局。  相似文献   

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体外受精-胚胎移植治疗过程中的心理护理   总被引:6,自引:0,他引:6  
目的探讨体外受精-胚胎移植(IVF—ET)治疗过程中实施心理护理与治疗成功率的关系。方法回顾性分析2000年1~12月在我院生殖中心接受IVF—ET治疗患者447例,共行482个周期,根据是否实施心理护理分组,A组为未实施心理护理组共169例,180个周期,B组为实施心理护理组共278例,302个周期。结果A组临床妊娠率为32.0%,流产率为24.1%;B组临床妊娠率为41.0%,流产率为18.4%。B组较A组妊娠率明显提高,流产率降低。结论适当的心理护理能有效地减轻患者的紧张情绪和思想压力,主动配合治疗,对提高IVF—ET的成功率有重要意义。  相似文献   

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吴佳烟  欧建平 《新医学》2022,53(9):630-634
胚胎移植并不仅是简单的胚胎转移。一次成功有效的胚胎移植,除了优质的胚胎、合适的宫腔环境,移植本身的技术性也占据着至关重要的地位,重视并掌握胚胎移植环节有助于提高体外受精-胚胎移植的成功率。该文主要就胚胎移植过程的相关技术方法及临床技巧在改善妊娠结局中的作用进行讨论,以期为临床实践者提供实用的参考建议。  相似文献   

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目的:分析不孕症患者体外受精-胚胎移植(In-vitro fertilization and embryo transfer,IVF-ET)妊娠结局的影响因素。方法:随机选取本院2016年4月至2017年4月收治的120例行体外受精-胚胎移植(IVF-ET)患者,根据妊娠是否成功,将其分为对照组(72例)、观察组(48例),即对照组为妊娠成功患者,观察组为妊娠未成功患者,比较两组病因、年龄、促性腺激素应用情况、卵巢功能水平、人绒毛膜促性腺激素水平、取卵情况、胚胎相关情况等差异,分析可以影响妊娠结局的因素。结果:妊娠成功患者72例,占比60.00%(72/120);妊娠未成功患者48例,占比40.00%(48/120)。通过分析发现,基本卵泡刺激素、年龄、周期次数,Cn时间、Cn剂量、HCG日黄体酮水平、受精率、卵子数、HCG日内膜厚度、优质胚胎数对比对照组明显优于观察组(P<0.05)。总结分析发现,不孕症患者的HCG日黄体酮水平、优质胚胎数、年龄是影响妊娠结局的主要因素。结论:在体外受精-胚胎移植治疗不孕症时,会受到患者自身多种因素的影响,从而降低妊娠率。  相似文献   

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目的 探讨卵巢颗粒细胞卵泡刺激素受体(FSHR)启动子突变与卵巢反应不良发生的分子机制.方法 对体外受精-胚胎移植(IVF-ET)周期中70例卵巢反应不良患者与88例卵巢正常反应患者FSHR 5'端起始位点的前263 bp DNA片段进行测序,研究卵巢颗粒细胞FSHR启动子突变与卵巢反应性的关系.结果 158例IVF患者中有63例发生-29位点G→A突变,发生率为40.0%;其中,卵巢反应不良组中该位点突变发生率[60.0%(42/70)]明显高于卵巢正常反应组[23.9%(21/88),χ2=21.450,P<0.01];而不同基因型组的基础卵泡刺激素值(bFSH)差异无统计学意义[G/G基因型组为(7.2±2.3)U/L,G/A和A/A基因型组为(7.1±2.0)U/L,t=0.457,P0.05];G/G基因型组的窦状卵泡数目[(14.2±1.3)个]明显高于G/A和A/A基因型组[(4.5±0.8)个,t=35.81,P<0.05];G/G基因型组采卵数[(14.0±1.2)个]明显高于G/A&A/A基因型组[(4.5±1.1)个,t=40.35,P<0.05];G/G基因型组雌二醇峰值[(2 865±557)pmol/L]明显高于G/A&A/A基因型[(880±211)pmol/L,t=25.80,P<0.05];G/G基因型组成熟卵子数[(13.6±1.2)个]明显高于G/A&A/A基因型组[(4.3±0.9)个,t=40.22,P<0.05].结论 FSHR启动子-29位点对PSHR启动子活性有显著影响,G→A突变可减弱启动子活性,使卵巢颗粒细胞对PSH反应不良.  相似文献   

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目的 探讨健康教育干预对不孕症患者体外受精-胚胎移植(IVF-ET)后受孕率的影响。方法 因不孕行体外受精-胚胎移植者420例,按取卵时单、双手术日分成实验组212例和对照组208例;对实验组入院后给予系统健康教育,对照组做一般常规介绍。结果 实验组妊娠率高于对照组(P〈0.05)。结论 健康教育有利于提高体外受精-胚胎移植术的妊娠率。  相似文献   

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Objective To sequence follicle stimulating hormone receptro (FSHR) promoter of the ovarian granulocyte and initially research the molecular mechanism of the poor ovarian response. Methods To study the relationship between FSHR promoter mutation of ovarian granulocyte and ovarian respone. The 263 bp DNA fragments before FSHR 5'initiation site in 70 cases of patients with poor ovarian respone and 88 cases of patients with ovarian normal respone who were in the cycle of IVF-ET were sequenced, Results There were 63 cases which occurred 29th site G → A point mutation in 158 women and the mutation rate was 40. 0%. Mutation rate [ 60. 0% ( 42/70 ) ] of 29th site G → A in group of poor ovarian respone was significantly higher(χ2 = 21. 450,P < 0. 01 ) than normal response group [ 23.9% ( 21/88 ) ]. There was no obviously variability ( t = 0. 457, P 0. 05 ) of basic FSH values between two groups [ G/G group was (7.2 ± 2. 3) U/L, G/A & A/A group was (7. 1±2. 0) U/L];there was obviously variability (t = 35. 81 ,P < 0. 05 ) in the number of follicles sinus between two groups ( G/G group was 14. 2±1.3, G/A & A/A group was 4. 5±0. 8 ) ;there was obviously variability ( t = 40. 35, P < 0. 05 ) in the number of ovum pick-up between two groups ( G/G group was 14. 0±1.2, G/A & A/A group was 4. 5±1.1 ) ;there was obviously variability (t =25. 80,P <0.05) of FE2-peak value between two groups [G/G group was (2 865±557) pmol/L, G/A & A/A group was (880±211 ) pmol/L] ;there was obviously variability (t =40. 22 ,P <0. 05) in the number of mature eggs ( G/G group was 13.6±1.2, G/A&A/Agroupwas4.3±0. 9).Conclusion The 29th site of FSHR promoter significantly affect the activity of FSHR promoter. Mutation of G→A can weaken promoter activity, so that ovarian granulocyte poor respone to FSH.  相似文献   

17.
Objective To sequence follicle stimulating hormone receptro (FSHR) promoter of the ovarian granulocyte and initially research the molecular mechanism of the poor ovarian response. Methods To study the relationship between FSHR promoter mutation of ovarian granulocyte and ovarian respone. The 263 bp DNA fragments before FSHR 5'initiation site in 70 cases of patients with poor ovarian respone and 88 cases of patients with ovarian normal respone who were in the cycle of IVF-ET were sequenced, Results There were 63 cases which occurred 29th site G → A point mutation in 158 women and the mutation rate was 40. 0%. Mutation rate [ 60. 0% ( 42/70 ) ] of 29th site G → A in group of poor ovarian respone was significantly higher(χ2 = 21. 450,P < 0. 01 ) than normal response group [ 23.9% ( 21/88 ) ]. There was no obviously variability ( t = 0. 457, P 0. 05 ) of basic FSH values between two groups [ G/G group was (7.2 ± 2. 3) U/L, G/A & A/A group was (7. 1±2. 0) U/L];there was obviously variability (t = 35. 81 ,P < 0. 05 ) in the number of follicles sinus between two groups ( G/G group was 14. 2±1.3, G/A & A/A group was 4. 5±0. 8 ) ;there was obviously variability ( t = 40. 35, P < 0. 05 ) in the number of ovum pick-up between two groups ( G/G group was 14. 0±1.2, G/A & A/A group was 4. 5±1.1 ) ;there was obviously variability (t =25. 80,P <0.05) of FE2-peak value between two groups [G/G group was (2 865±557) pmol/L, G/A & A/A group was (880±211 ) pmol/L] ;there was obviously variability (t =40. 22 ,P <0. 05) in the number of mature eggs ( G/G group was 13.6±1.2, G/A&A/Agroupwas4.3±0. 9).Conclusion The 29th site of FSHR promoter significantly affect the activity of FSHR promoter. Mutation of G→A can weaken promoter activity, so that ovarian granulocyte poor respone to FSH.  相似文献   

18.
Objective To sequence follicle stimulating hormone receptro (FSHR) promoter of the ovarian granulocyte and initially research the molecular mechanism of the poor ovarian response. Methods To study the relationship between FSHR promoter mutation of ovarian granulocyte and ovarian respone. The 263 bp DNA fragments before FSHR 5'initiation site in 70 cases of patients with poor ovarian respone and 88 cases of patients with ovarian normal respone who were in the cycle of IVF-ET were sequenced, Results There were 63 cases which occurred 29th site G → A point mutation in 158 women and the mutation rate was 40. 0%. Mutation rate [ 60. 0% ( 42/70 ) ] of 29th site G → A in group of poor ovarian respone was significantly higher(χ2 = 21. 450,P < 0. 01 ) than normal response group [ 23.9% ( 21/88 ) ]. There was no obviously variability ( t = 0. 457, P 0. 05 ) of basic FSH values between two groups [ G/G group was (7.2 ± 2. 3) U/L, G/A & A/A group was (7. 1±2. 0) U/L];there was obviously variability (t = 35. 81 ,P < 0. 05 ) in the number of follicles sinus between two groups ( G/G group was 14. 2±1.3, G/A & A/A group was 4. 5±0. 8 ) ;there was obviously variability ( t = 40. 35, P < 0. 05 ) in the number of ovum pick-up between two groups ( G/G group was 14. 0±1.2, G/A & A/A group was 4. 5±1.1 ) ;there was obviously variability (t =25. 80,P <0.05) of FE2-peak value between two groups [G/G group was (2 865±557) pmol/L, G/A & A/A group was (880±211 ) pmol/L] ;there was obviously variability (t =40. 22 ,P <0. 05) in the number of mature eggs ( G/G group was 13.6±1.2, G/A&A/Agroupwas4.3±0. 9).Conclusion The 29th site of FSHR promoter significantly affect the activity of FSHR promoter. Mutation of G→A can weaken promoter activity, so that ovarian granulocyte poor respone to FSH.  相似文献   

19.
Objective To sequence follicle stimulating hormone receptro (FSHR) promoter of the ovarian granulocyte and initially research the molecular mechanism of the poor ovarian response. Methods To study the relationship between FSHR promoter mutation of ovarian granulocyte and ovarian respone. The 263 bp DNA fragments before FSHR 5'initiation site in 70 cases of patients with poor ovarian respone and 88 cases of patients with ovarian normal respone who were in the cycle of IVF-ET were sequenced, Results There were 63 cases which occurred 29th site G → A point mutation in 158 women and the mutation rate was 40. 0%. Mutation rate [ 60. 0% ( 42/70 ) ] of 29th site G → A in group of poor ovarian respone was significantly higher(χ2 = 21. 450,P < 0. 01 ) than normal response group [ 23.9% ( 21/88 ) ]. There was no obviously variability ( t = 0. 457, P 0. 05 ) of basic FSH values between two groups [ G/G group was (7.2 ± 2. 3) U/L, G/A & A/A group was (7. 1±2. 0) U/L];there was obviously variability (t = 35. 81 ,P < 0. 05 ) in the number of follicles sinus between two groups ( G/G group was 14. 2±1.3, G/A & A/A group was 4. 5±0. 8 ) ;there was obviously variability ( t = 40. 35, P < 0. 05 ) in the number of ovum pick-up between two groups ( G/G group was 14. 0±1.2, G/A & A/A group was 4. 5±1.1 ) ;there was obviously variability (t =25. 80,P <0.05) of FE2-peak value between two groups [G/G group was (2 865±557) pmol/L, G/A & A/A group was (880±211 ) pmol/L] ;there was obviously variability (t =40. 22 ,P <0. 05) in the number of mature eggs ( G/G group was 13.6±1.2, G/A&A/Agroupwas4.3±0. 9).Conclusion The 29th site of FSHR promoter significantly affect the activity of FSHR promoter. Mutation of G→A can weaken promoter activity, so that ovarian granulocyte poor respone to FSH.  相似文献   

20.
Objective To sequence follicle stimulating hormone receptro (FSHR) promoter of the ovarian granulocyte and initially research the molecular mechanism of the poor ovarian response. Methods To study the relationship between FSHR promoter mutation of ovarian granulocyte and ovarian respone. The 263 bp DNA fragments before FSHR 5'initiation site in 70 cases of patients with poor ovarian respone and 88 cases of patients with ovarian normal respone who were in the cycle of IVF-ET were sequenced, Results There were 63 cases which occurred 29th site G → A point mutation in 158 women and the mutation rate was 40. 0%. Mutation rate [ 60. 0% ( 42/70 ) ] of 29th site G → A in group of poor ovarian respone was significantly higher(χ2 = 21. 450,P < 0. 01 ) than normal response group [ 23.9% ( 21/88 ) ]. There was no obviously variability ( t = 0. 457, P 0. 05 ) of basic FSH values between two groups [ G/G group was (7.2 ± 2. 3) U/L, G/A & A/A group was (7. 1±2. 0) U/L];there was obviously variability (t = 35. 81 ,P < 0. 05 ) in the number of follicles sinus between two groups ( G/G group was 14. 2±1.3, G/A & A/A group was 4. 5±0. 8 ) ;there was obviously variability ( t = 40. 35, P < 0. 05 ) in the number of ovum pick-up between two groups ( G/G group was 14. 0±1.2, G/A & A/A group was 4. 5±1.1 ) ;there was obviously variability (t =25. 80,P <0.05) of FE2-peak value between two groups [G/G group was (2 865±557) pmol/L, G/A & A/A group was (880±211 ) pmol/L] ;there was obviously variability (t =40. 22 ,P <0. 05) in the number of mature eggs ( G/G group was 13.6±1.2, G/A&A/Agroupwas4.3±0. 9).Conclusion The 29th site of FSHR promoter significantly affect the activity of FSHR promoter. Mutation of G→A can weaken promoter activity, so that ovarian granulocyte poor respone to FSH.  相似文献   

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