Objective:To investigate the role of the deubiquitinase Cylindromatosis (CYLD) in aging of mouse cardiomyocytes and the underlying mechanism.Methods:Wild-type (WT) FVB mice and CYLD-overexpressing (CYLD +/+) mice were used to establish mice models of natural aging. Then, 2-month-old male wild-type FVB mice (WT-2M, n=10) and CYLD +/+ mice (CYLD-2M, n=10) were assigned to the young age group, and those routinely raised for 17.5 months (WT-17.5M, CYLD-17.5M, n=10 each) to the old age group. Small animal ultrasonography was used to measure the cardiac function (LVEF, LVFS), Western blotting was used to examine the expression of aging-related proteins p53, p21, and p16 in myocardial tissues, and qPCR was used to determine the transcription of senescence associated secretory phenotypes (SASP) interlenkin-1β (IL-1β), matrix metalloproteinase 3 (MMP3) and CXC chemokine ligand 1 (CXCL1) in myocardial tissues. Transcriptome sequencing was used to detect the signaling pathways by which CYLD regulates cardiomyocyte senescence. Tumor necrosis factor-α (TNF-α) pathway was verified by qPCR. Results:Compared with WT-17.5M mice, CYLD-17.5M mice presented better cardiac function with higher values of LVEF and LVFS (all P<0.05), lower expression levels of p53, p21, and p16 proteins (all P<0.05), and less transcription of IL1B, MMP3, and CXCL1 (all P<0.05). Compared with WT-2M mice, the WT-17.5M mice had significantly higher expression of p53, p21 and p16 proteins (all P<0.01), and up-regulated transcription levels of IL1B, MMP3 and CXCL1 (all P<0.01). Transcriptome sequencing showed 64 up-regulated signaling pathways in WT-17.5M mice when comparing to WT-2M mice, and 37 down-regulated signaling pathways in CYLD-17.5M mice when comparing to WT-17.5M mice; there were 29 pathways with differential signaling when comparing CYLD-17.5M to WT-17.5M mice. qPCR with TNF-α pathway selected for verification showed significantly increased TNF-α transcription in WT-17.5M mice than in WT-2M mice and CYLD-17.5M mice (all P<0.05) . Conclusion:CYLD plays a protective role in natural cardiomyocyte senescence. Mediation of the TNF-α pathway may be one of mechanisms underlying the effect of CYLD against myocardial aging.
目的:探讨NSUN2 对阿霉素(doxorubicin,DOX)诱导H9C2 细胞损伤的作用及可能机制.方法:H9C2细胞分两组,对照组(加入 0.9%氯化钠溶液 2 μL)和DOX组(加入用 0.9%氯化钠溶液配置成 0.5 mg/mL阿霉素 2 μL、siNSUN2 转染H9C2 细胞、腺病毒转染人源NSUN2 建立NSUN2 稳定过表达H9C2 细胞系,加入阿霉素 500 ng/mL共培养 24h后,用DCFH-DA探针、Western blot、免疫荧光、TUNEL染色等方法检测细胞的活性氧(ROS)、凋亡及NSUN2 的变化,ELISA检测细胞培养基上清内NSUN2 表达变化.结果:Western blot结果显示,DOX组与对照组比较,H9C2 细胞Bax蛋白水平及NSUN2 表达水平升高(P<0.01),Bcl-2 蛋白水平下降(P<0.01);ELISA检测细胞培养液内NSUN2 表达水平DOX组较对照组升高(P<0.05);TUNEL结果显示DOX组细胞凋亡明显增加;DCFH-DA探针检测DOX组细胞内ROS水平较对照组明显升高;H9C2 细胞敲减NSUN2 后,DOX组细胞内Bax蛋白水平较对照组升高(P<0.01),Bcl-2 蛋白表达水平下降(P<0.01);NSUN2 过表达时,DOX组与对照组比较,细胞内Bax表达水平下降(P<0.01),Bcl-2 表达水平升高(P<0.01).结论:NSUN2 能抑制阿霉素诱导的H9C2 细胞损伤,对其H9C2 细胞起保护作用,机制可能与NSUN2 抗氧化应激相关.
目的 探讨甲基转移酶样蛋白7B(METTL7B)对人肝细胞脂滴形成的影响.方法 取5只8~10周龄雄性C57BL/6J小鼠的心、肝、脑、肺、肾、肌肉、皮肤等组织,检测组织中METTL7B蛋白表达情况.用不同浓度油酸(0、0.25、0.5、1.0 mmol/L)处理人正常肝细胞LO2,采用CCK-8法检测细胞活力,油红O染色检测细胞内脂滴含量.METTL7B siRNA转染LO2细胞,检测LO2细胞内脂滴含量以及三酰甘油和胆固醇代谢相关基因的表达情况.结果 METTL7B蛋白在小鼠肝脏组织中表达最高,在其他器官组织中表达较弱或不表达.与油酸0 mmol/L比较,油酸1.0 mmol/L能降低细胞活力(P<0.05).油酸0.5 mmol/L处理后,细胞内脂滴含量增多,且脂滴大小清晰,METTL7B mRNA和蛋白表达升高(P<0.05).干扰METTL7B后,细胞内脂滴含量减少(P<0.05),三酯甘油代谢相关基因载脂蛋白B100、Runt相关转录因子2、硬脂酰辅酶A去饱和酶mRNA表达上调(P<0.05),胆固醇代谢相关基因肉毒碱棕榈酰转移酶、胆固醇调节元件结合蛋白1(SREBP1)、SREBP2 mRNA表达下调(P<0.05).结论 METTL7B与人肝细胞脂滴形成密切相关,主要通过上调三酰甘油代谢相关基因和下调胆固醇代谢相关基因的表达来发挥作用.
目的 研究小鼠急性心肌梗死(AMI)后不同时间点心肌组织自噬水平的动态变化.方法 选取8~10周龄SPF级C57BL/6J野生型小鼠40只,随机分为假手术组(Sham组)、AMI组(永久结扎左前降支),每组20只,分别于术后7、14、28 d时,用心脏超声检测心脏功能及结构变化,Masson染色观察小鼠梗死周边心肌组织纤维化,Western blot检测自噬蛋白、透射电镜观察自噬小体、免疫组织化学检查凋亡蛋白表达.结果 Masson染色显示,AMI组梗死周边组织间质纤维化随着时间的推移加重;AMI组7、14和28 d时Bax蛋白较Sham组明显上调(0.71±0.08、0.77±0.05和0.86±0.06 vs 0.53±0.08,P<0.05),Bcl-2和自噬微管相关蛋白轻链3蛋白降低(P<0.05),P62蛋白表达增强(P<0.05);透射电镜示,AMI组梗死周边心肌组织内 自噬小体数量明显减少.结论 小鼠AMI后梗死周边心肌组织自噬水平进行性降低,心室重构进一步恶化,自噬可能在AMI中起保护作用.
Objective:To explore the clinical application value of metagenomics next-generation sequencing (mNGS) in assisting the diagnosis of invasive fungal diseases, and to provide pathogenic evidence for the clinical diagnosis and treatment of mucormycosis.Methods:The alveolar lavage fluid of a patient with unexplained lung infection was detected by mNGS to determine the pathogen, and the treatment plan was adjusted according to the mNGS test report.Results:The patient had intermittent chest pain and cough for longer than 5 months. The chest CT showed multiple shadows and cavities in both lungs. There was no abnormality in routine laboratory and pathogenic examinations, and no significant improvement was found after various anti-infection treatments. The mNGS of alveolar lavage fluid submitted for examination revealed that the pathogen was Lichtheimia ramose. After switching to amphotericin B for anti-infection treatment, the patient’s infected lesions shrank and the symptoms relieved significantly.Conclusions:mNGS is an important auxiliary diagnostic method to identify rare pathogens, which is of great significance to assist the diagnosis of lung invasive mycosis.
Objective:To investigate the clinical and pathogenic characteristics of Bordetella parapertussis infection.Methods:Clinical data of the patient who was admitted to the First People’s Hospital of Tianmen City was collected, the disease course records of this patient and the laboratory isolation and identification process of the pathogenic bacteria were analyzed and the relevant literatures were reviewed.Results:This child, female, 1 year and 3 months old, with clinical manifestations such as cough and shortness of breath, mild inspiratory trigeminal sign, coarse breath sounds in both lungs, moderate croup and a few wet rales could be heard; laboratory examination results showed that white blood cells: 12.49 × 109/L, red blood cells: 4.36 × 1012/L, neutrophil percentage: 58.4%, platelets: 260 × 109/L, serum iron: 7.5 μmol/L, creatinine: 26.5 μmol/L, total carbon dioxide: 19.6 mmol/L, total calcium: 2.76 mmol/L, hydroxybutyate dehydrogenase: 291 U/L, lactate dehydrogenase: 310 U/L, creatine kinase isoenzyme: 25.20 U/L, creatine kinase: 308 U/L; Mycoplasma pneumoniae IgM antibody: weakly positive. The patient’s chest CT imaging showed a sheet of high-density film of the right upper lung. The sputum culture isolates were identified as Bordetella parapertussis by protein time-of-flight mass spectrometry (MALDI-TOF MS). The child was discharged from hospital after anti-infection treatment.Conclusion: Bordetella parapertussis infection is relatively rare, and early pathogen diagnosis is important for effective treatment.
目的 分析小鼠心肌梗死(MI)后7、14、28d心肌组织mRNA表达谱的变化.方法 将C57BL/6J小鼠随机分为假手术组(S组)和MI模型组(MI组),每组10只.采用结扎小鼠冠状动脉左前降支方法建立MI模型,行心电图和组织病理学检查验证,心脏彩超观察心脏结构变化.取梗死边缘区心肌组织进行转录组测序,筛选差异表达mRNA基因,采用基因本体(GO)分析和京都基因与基因组百科全书(KEGG)分析参与重要信号通路的差异表达基因.结果 MI组建模后3个时间点左心室舒张末期内径及其容积、左心室收缩末期内径及其容积均大于S组,而左心室射血分数低于S组(P<0.05).MI组建模后3个时间点共280个基因均表达上调,而40个基因均表达下调.GO分析显示,持续表达上调或下调的基因主要参与的生物功能为生物调节、对刺激的反应、代谢过程、发育过程等;细胞成分有细胞膜、细胞核、囊泡、细胞外基质等;分子功能有蛋白结合、转运激活等.KEGG分析显示,持续表达上调的基因参与信号通路多促进心室重塑,持续表达下调的基因参与信号通路多抑制和延缓心室重塑.结论 小鼠MI建模后心脏形态结构发生异常,心功能减低;不同时间点进行mRNA谱分析显示涉及基因数目众多且功能复杂.
Objective:To investigate the diagnostic characteristics of facial abscess caused by Streptococcus constellatus.Methods:The clinical data of a case of facial abscess caused by Streptococcus constellatus admitted to the Oncology Department of Tianmen First People′s Hospital on June 27, 2020 were retrospectively analyzed, and the relevant literatures were reviewed.Results:The patient presented with a mass in the right maxillofacial region, with partial skin ulceration and purulent discharge. The patient had an anamnesis of nasopharyngeal carcinoma. Imaging indicated right middle ear mastoiditis and sinusitis. Laboratory examination found that IgA antibody of human herpesvirus was weakly positive, C-reactive protein level was 11.07 mg/L, procalcitonin level was 1.26 μg/L, blood culture was negative, and Streptococcus constellatus was detected in wound secretion. The pathogen was resistant to erythromycin and clindamycin.Conclusions:As a kind of opportunistic pathogen, Streptococcus constellatus can cause suppurative infection in various tissues and organs of human body, which should arouse clinical attention. We should improve the detection rate of pathogenic bacteria, so as to achieve early diagnosis and treatment.
分子生物学检验实验课是医学检验专业本科生的必修主干科目,为提高教学质量,我们需要重视实验教学各环节,丰富教学内容,对学生严格要求,督促他们多动手、动脑,以加深对学生理论知识的理解,并提高其解决临床问题的能力.
啮蚀艾肯菌是一种条件致病菌,在临床感染中比较少见,国内也只有零星报道。该菌可存在于人呼吸道、消化道、口腔、泌尿道等黏膜表面,当人体免疫力低下或黏膜表面破损时,常引起软组织脓肿、脑膜炎、脑脓肿、颈部脓肿及腹部感染等。该菌营养要求高,生长缓慢,培养困难,容易漏检、漏诊,应引起微生物实验室检验人员的注意。本文报道1例由啮蚀艾肯菌引起的颈部脓肿,最终行手术并抗感染治疗后痊愈的病例。
目的 通过对HeLa细胞过表达TET1基因,探究TET1基因对宫颈癌细胞增殖迁移能力的影响.方法 采用TALE-VP64系统构建TET1过表达质粒,转染宫颈癌HeLa细胞,四唑盐(MTT)比色法监测细胞增殖状况,划痕试验检测细胞迁移能力的变化,Transwell试验检测HeLa细胞侵袭能力的变化.结果 MTT法检测HeLa细胞增殖状况,TET1过表达的Clone 1和Clone 2细胞增殖能力明显弱于野生型HeLa细胞(P<0.05).Transwell试验检测TET1过表达Clone 1及Clone 2 HeLa细胞穿过magtrigel胶及小室的数量分别是(21±5)和(22±6)个/视野,而野生型HeLa细胞组为(38±7)个/视野,与野生型HeLa细胞组比较,差异有统计学意义(P<0.05).划痕试验检测TET1过表达组(Clone 1、Clone 2)细胞和野生型HeLa组细胞24 h及48 h的迁移率,后者明显高于前者(P<0.01).TET1过表达能够抑制HeLa细胞的增殖、侵袭、迁移等能力.结论 TET1基因过表达对宫颈癌HeLa细胞有抑癌基因的作用.
目的 研究益母草注射液对子宫缺血再灌注损伤的保护作用机制.方法 Wistar雌性大鼠30只,取其中20只采用线栓法结扎大鼠腹腔动脉30 min后再灌注60 min的方法建立子宫缺血再灌注损伤模型并均分为模型组和益母草组,另10只设为对照组作为正常对照.益母草组按6 mg/(kg·d)剂量腹腔注射给予益母草注射液,模型组和对照组腹腔注射给予生理盐水对照.治疗7d后取大鼠子宫组织,采用考马斯亮蓝染色试剂盒(常规法)检测子宫组织高能磷酸化合物中三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、磷酸腺苷(AMP)和总腺嘌呤核苷酸(TAN)含量;采用离子交换柱层析法检测乳酸脱氢酶(LDH)水平;采用黄嘌呤氧化酶法检测子宫组织中超氧化物歧化酶(SOD);采用硫代巴比妥酸法检测子宫组织中丙二醛(MDA)水平.用垂体后叶素灌流3组大鼠离体子宫,然后分别加入益母草注射液灌流,比较3组大鼠离体子宫平滑肌的收缩强度、收缩频率并计算子宫活动力.结果 与模型组比较,益母草组子宫组织中ATP、ADP、AMP、TAN和SOD明显升高,LDH和MDA明显降低(P<0.05);垂体后叶素可引起3组大鼠子宫收缩,其中对照组对垂体后叶素最为敏感,其次为益母草组,模型组次之;益母草注射液可明显增强垂体后叶素引起的子宫收缩,益母草组子宫收缩强度、收缩频率和子宫活动力均明显高于模型组(P<0.05).结论 益母草注射液可增强组织供能并促进组织能量代谢、提高缺血再灌注离体子宫对垂体后叶素的敏感性并抑制子宫缺血再灌注后的氧化应激反应,对大鼠子宫缺血-再灌注损伤具有保护作用.
目的 观察益母草注射液对缺血再灌注大鼠离体子宫能量代谢及子宫活动力的影响.方法 雌性SD大鼠40只,将30只大鼠随机均分为模型组、缩宫素组和益母草组,3组均采用线栓法构建子宫缺血再灌注损伤模型,于阻断子宫血供30 min再灌注45 min后取子宫分别进行灌流,另取10只不手术建模(假手术组).记录4组大鼠离体子宫平滑肌的收缩频率、收缩张力和子宫活动力.比较灌流后离体子宫平滑肌高能磷酸化合物(Energy rich phosphate compounds,EPC)水平及离体子宫平滑肌标本线粒体呼吸链酶复合体Ⅰ~Ⅳ和钙离子(Ca2+)浓度.结果 益母草组离体子宫平滑肌收缩张力、收缩频率和子宫活动力均明显升高,但没有恢复到假手术组水平,与假手术组和模型组比较差异有统计学意义(P<0.05);Ca2+浓度明显升高,与模型组比较差异有统计学意义(P<0.05).益母草组三磷酸腺苷(Adenosine triphosphate,ATP)、二磷酸腺苷(Adenosine diphosphate,ADP)、磷酸腺苷(Adenosine monophosphate,AMP)、总腺嘌呤核苷酸(Total adenine nucleotides,TAN)及线粒体呼吸链酶复合体Ⅰ~Ⅳ明显升高,与模型组和缩宫素组比较差异有统计学意义(P<0.05).结论 益母草注射液可能通过开放Ca2+通道增强离体子宫平滑肌对益母草注射液的敏感性,并通过促进能量代谢发挥对缺血再灌注子宫的保护作用.
Objective:To investigate the effect of autophagy on cervical cancer cells stemness and its proliferation ability.Methods:HeLa mammospheres were isolated with the method of suspension culture.Formation of autophagosome was observed by staining with acridine orange under fluorescence microscope.Western blot was used to detect the expression of Beclin1 and LC3B in HeLa adherent cells and mammospheres.After starvation induction with EBSS in HeLa adherent cells and mammospheres for 4 hours and 8 hours,formation of autophagosome was observed by staining with acridine orange under fluorescence microscope;Western blot was used to detect the expression of Beclin1 and LC3B,proliferative ability of wild type HeLa cells and starvation-stimulated HeLa cells was detected using a real-time cell-based assay system.After inhibiting the autophagy with 3-methyladenine(3-MA) in HeLa adherent cells and mammospheres,Western blot was used to detect the expression of Beclinl and LC3B and proliferative ability of wild type HeLa cells and 3-MA-stimulated HeLa cells was detected using a real-time cell-based assay system.CRISPR/Cas9 gene editing techniques was used to down regulate the expression of Beclin1,proliferative ability of wild type HeLa cells and Beclin1-mutated HeLa cells was detected using a real-time cell-based assay system.Results:Compared with HeLa adherent cells,HeLa mammospheres had higher basic levels of autophagy.And the autophagy level was higher in HeLa mammospheres than in adherent cells under the starvation conditions.The autophagy level is significantly higher after 4 hours starvation induction both in the mammospheres and the adherent cells,which was confirmed by western blot analysis and acridine orange fluorescent staining.The proliferative ability of starvation inducted HeLa cells were weakened compared with that of wild type HeLa cells and it's more obvious at 8 hours.The expression of Beclin1 and LC3B are lower in the presence of 3-MA and it's more obvious in adherent cells.The proliferative ability of HeLa cells were also weakened in the presence of 3-MA.Additionally,the proliferative ability of Beclin1-mutated HeLa cells were elevated compared with that of wild type HeLa cells.Conclusion:Autophagy is involved in maintaining the stemness of cervical cancer cells.Significantly,autophagy also can have an impact on the proliferative ability of cervical cancer cells.Gene targeting-induced disruption of autophagy key gene Beclin1 and LC3B to alter autophagy can be a promising therapeutic strategy for curing cervical cancer.
Objective:Recently modification of CCR5 locus for anti-HIV-1 infection was performed by the genome editing methods like TELENs or CRISPR-Cas with the strategies of disruption of CCR5.To obtain the exact mutation of Δ32 deletion at the locus,we employed a novel strategy for developing CCR5Δ32 targeting vector based on Red/ET homologous recombination.Methods:Firstly,a rpsl-neo cassette flanked by two homology arms to CCR5 was amplified by PCR and then electroporated into E.coli DH10B with the BAC bearing CCR5.Through Red/ET homologous recombination,a 52 bp DNA sequences containing Δ32 in CCR5 was replaced by rpsl-neo.Subsequently,a non-selectable fragment was electroporated and replaced the rpsl-neo resulting in Δ32 deletion at CCR5.Furthermore,a loxp-neo-loxp cassette was also introduced into intron 2 within CCR5 through the same machnism,which allows for G418 selection for future targeting human cells and will be cut under the Cre protein only leaving one loxp at the intron region.Results:rpsl-neo cassette was successfully inserted into CCR5 on BAC and replaced by non-selectable fragment and at the same time a loxp-neo-loxp cassette was also introduced into intron 2 of CCR5.Conclusion:CCR5Δ32-loxp-neo-loxp targeting vector was accessed by Red/ET homologous recombination.
Objective To investigate the effect of autophagy on the proliferation and migration of cervi-cal cancer cells ,as well as the underlining mechanisms .Methods Rapamycin was used to induce the autophagy in HeLa cells,formation of autophagosomes was observed by staining with acridine orange under fluorescence mi -croscope.Western blot was used to detect the expression of LC 3 and PI3K/Akt/mTOR in HeLa cells.The LC3 plasmid was transfected into HeLa cells .The distribution of LC3 in cells and the expression of LC3 was identified by fluorescence microscope and Western blot ,respectively.The autophagy was inhibited with 3-methyladenine(3-MA )in HeLa cells.The cell proliferation was monitored by RTCA real -time instrument.Transwell chamber was carried out to assess cell migration .Results After 6h of rapamycin treatment ,the expression of LC3B was in-creased in HeLa cells ( P<0 .05 ) .The proliferative and migration ability were weakened compared to wild type HeLa cells(P<0.05).The same results in the presence of 3-MA.The expression of PI3K/AKT/mTOR path-way proteins were activated by rapamycin treatment and LC 3 overexpression(P<0.05).Conclusion Autophagy can suppress the proliferation and migration in cervical cancer cells ,which may relate to PI3K/Akt/mTOR path-way.
目的 探讨CXC趋化因子-4受体(CXCR4)表达上调对U251细胞增殖、侵袭及迁移能力的影响及其作用机制.方法 构建携带CXCR4基因的质粒,采用电转染法将携带CXCR4基因的质粒整合到胶质瘤U251细胞的基因组中,然后将细胞分为空白对照组、阴性对照组和CXCR4上调组,分别从mRNA水平和蛋白水平检测CXCR4及其他相关基因的表达;MTT试验检测细胞增殖能力的改变;划痕试验检测细胞的迁移能力;Transwell侵袭试验检测细胞侵袭性的变化.结果 与空白对照组和阴性对照组相比,CXCR4上调组U251细胞CXCR4在mRNA和蛋白水平上表达都增强,细胞增殖、侵袭和迁移能力均显著增强;而空白对照组和阴性对照组之间并无明显变化.结论 CXCR4在胶质瘤的增殖、侵袭、迁移行为中发挥着重要的作用,可以被视为胶质瘤治疗的靶向基因.
Objective To construct the HeLa stable expressing cell line expressed by FAM92A1-289 and to observe its function on cell proliferation.Methods We constructed the recombinant expression vector CMV-SP6-TALEN-GFP-289, then transfected it into HeLa cells.We obtained the stable expressing cells HeLa/289 of FAM92A1-289 by puromycin screen-ing.Scratch assay colony-formation assay and MTT assay were used to detect the changes in migration, tumor growth rate and survival rate of HeLa/289 cells.Results The cervical cancer HeLa stable expressing cell line over-expressing FAM92A1-289 was successfully constructed.After detection, the migration ability was stronger, rate of growth was faster and the survival rate was higher.Conclusion The stable expressing cells HeLa/289 of FAM92A1-289 were established succesfully. FAM92A1-289 gene has the effect of promoting cell proliferation, and it is the related gene regulating the cell proliferation.
Objective: To investigate whether butyl hydroxyanisole(BHA) and β-mereaptoethanol(β-ME) could be used to induce human umbilical cord mesenchymal stem cells(hUC-MSCs) into neural cells.Methods: The normal cultured fourth passage hUC-MSCs were randomly divided into experiment group and control group.The experiment group were induced by 200 μmol·L-1 BHA+2 mmol·L-1β-ME,and the control group were continuously cultured with common MSC medium.The morphologic changes of cells were observed every 12 hours.The cells of the two groups were collected after 24 h and 72 h distinctively to extract total RNA and analyzed neural cell specific genes by RT-PCR.On the third day after induction,the expressions of nestin,glial fibrillary acidic protein(GFAP) and neuron-specific enolase(NSE) were detected by immunohistochemistry.Results: Within 12 hours of induction,some of the hUC-MSCs assumed neuronal morphology,the cell became smaller,diacaustic was higher.These changes became more and more obvious as the time being.After induction for 72 h,a large number of responsive cells exhibited typical neuronal morphology.Nestin,GFAP and NSE were immunepositive.RT-PCR indicated that nestin,MAP and NF-L began to express 24 h after induction.72 h later,the expression of nestin and NF-L were reduced,while MAP and NeuroD1 expression became increased.Conclusion: BHA can induce hUC-MSCs differentiated into neural cells quickly.
目的 探讨载脂蛋白C3(APOC3)-455T>C基因多态性与湖北汉族人群代谢综合征(MS)及血脂的关系.方法 采集226例MS患者和258名健康者(对照组)血液用聚合酶链反应限制性片段长度多态性(PCR-RFLP)分析APOC3-455T>C基因多态性的分布,并检测其血脂和血糖水平.结果 -455C等位基因在MS与对照组中的分布频率不同,差异有统计学意义(P<0.05).两组中C等位基因携带者三酰甘油(TG)水平比TT纯合子者高(P<0.05),而高密度脂蛋白胆固醇(HDL-C)水平比TT纯合子者低.APOC3等位基因是MS独立影响因子(OR=1.987,P=0.038).结论 POC3-455T>C基因多态性与血脂水平特别是TG及HDL-C有关,APOC3-455C等位基因可能为MS的危险因素.