简介:[ 摘要 ] 采用膨胀法,结合金相法,测试了实验钢的临界转变点 Ac1 、 Ac3 及 Ms 点。测定了不同冷却温度下轧辊用钢 的膨胀曲线,得到了该材料的连续冷却转变曲线( CCT )。并根据温度对连续冷却转变过程中相转变的影响进行了探讨。
简介:摘要目的探讨1例Bweak亚型个体的分子机制。方法选取2016年12月5日于浙江省血液中心献血的1例受试者为研究对象。利用血清学方法鉴定受试者的ABO表型,用体外酶活性试验测定其血清中B糖基转移酶(GTB)的活性。用PCR扩增ABO基因第5 ~ 7外显子及侧翼序列并确定其基因型,采用T-A克隆技术分离单倍体并进行测序验证。用ProtParam和PSIPRED软件分析蛋白的一级理化性质和二级结构。用PolyPhen-2、SIFT、PROVEAN三种软件分析错义变异对蛋白的作用效应。结果受试者血清学检测为Bweak亚型,血清中存在抗B抗体。体外酶活性试验显示其GTB活性显著降低。单倍体克隆测序分析发现B等位基因上存在c.398T>C错义变异,为一个新的B等位基因,可导致GTB第133位的苯丙氨酸替换为丝氨酸(p.Phe133Ser)。生物信息学分析提示上述替换对蛋白的一级和二级结构影响不明显,但变异蛋白的热力学能量增加6.07 kcal/mol,严重降低了热稳定性,生物信息学预测该变异对蛋白功能有害。结论新等位基因ABO*B.01-398C是引起Bweak亚型抗原弱表达的机制,生物信息学分析有助于评估其结构和功能的变化。
简介:Bothendotheliallipasegene(LIPG)584C>T(rs2000813)polymorphismandalcoholconsumptionmodulateserumlipidlevels.Buttheirinteractionsonserumlipidprofilesarenotwellknown.ThepresentstudywasundertakentodetecttheinteractionsofLIPG584C>Tpolymorphismandalcoholconsumptiononserumlipidlevels.GenotypingoftheLIPG584C>Twasperformedin763nondrinkersand520drinkersaged15-85.Interactionsbetweenthegenotypesandalcoholconsumptionwereassessedbyusingacross-productterm.Thelevelsofserumtotalcholesterol(TC),triglyceride(TG),high-densitylipoproteincholesterol(HDL-C),apolipoprotein(Apo)AI,andtheratioofApoAItoApoBwerehigherindrinkersthaninnondrinkers(P<0.01forall).Therewasnosignificantdifferenceinthegenotypicandallelicfrequenciesbetweennondrinkersanddrinkers.ThelevelsofserumTC,HDL-CandApoAIinnondrinkersweredifferentamongthethreegenotypes(P<.05-.01).ThesubjectswithCTgenotypehadhigherserumTC,HDL-CandApoAIlevelsthanthesubjectswithCCgenotype.ThelevelsofserumHDL-CandApoAIindrinkersweredifferentamongthethreegenotypes(P<.001andP<.05;respectively).TheindividualswithTTgenotypehadhigherserumHDL-CandApoAIlevelsthantheindividualswithCCandCTgenotypes.ThelevelsofTCinnondrinkerswerecorrelatedwithLIPG584C>Tallele(P<.05),whereasthelevelsofTGandHDL-CwereassociatedwithLIPG584C>Talleles(P<.05)andgenotypes(P<.05);respectively.ThepresentstudysuggeststhatthesubjectswithTTgenotypebenefitedmorefromalcoholconsumptionthanthesubjectswithCTandTTgenotypesinincreasingserumHDL-CandApoAIlevels.