目的探讨振幅整合脑电图(aEEG)评分联合血清脑红蛋白对晚期早产儿脑损伤情况诊断价值。方法回顾性分析2018年1月至2019年12月在邢台市第三医院接受治疗的晚期早产儿133例临床资料。收集患儿aEEG、血清脑红蛋白及早期新生儿神经学评分新...目的探讨振幅整合脑电图(aEEG)评分联合血清脑红蛋白对晚期早产儿脑损伤情况诊断价值。方法回顾性分析2018年1月至2019年12月在邢台市第三医院接受治疗的晚期早产儿133例临床资料。收集患儿aEEG、血清脑红蛋白及早期新生儿神经学评分新生儿20项行为神经测定(NBNA)检测结果。依据判断结果将患者分为脑损伤组(n=45)与无脑损伤组(n=88),比较2组患儿aEEG评分、血清脑红蛋白、NBNA评分,并对aEEG评分、血清脑红蛋白与NBNA评分进行相关性分析。以ROC法判断aEEG评分联合血清脑红蛋白对晚期早产儿脑损伤的诊断价值。结果2组患儿胎龄、性别、分娩方式及出生体质量比较差异无统计学意义(P>0.05)。脑损伤组患儿aEEG评分(7.68±2.04 vs 9.92±3.11)、NBNA评分(33.05±7.14 vs 37.29±2.19)均显著低于无脑损伤组(P<0.01),血清脑红蛋白显著高于无脑损伤组[(158.28±42.09)mg/L vs(119.36±31.84)mg/L,P<0.01]。相关性分析结果显示,aEEG评分与NBNA评分呈显著正相关(r=0.639,P<0.05),血血清脑红蛋白与NBNA评分呈显著负相关关系(r=-0.698,P<0.05)。ROC分析结果显示,aEEG评分对晚期早产儿脑损伤早期诊断cut-off值为10分,AUC为0.893,95%CI为0.830~0.955,敏感度为77.78%,特异性为80.68%;血清脑红蛋白cut-off值为129.71 mg/L,AUC为0.815,95%CI为0.704~0.885,敏感度为73.33%,特异性为84.09%;联合诊断可有效提高诊断敏感度(P<0.05)。结论晚期早产儿脑损伤可引起aEEG评分及血清脑红蛋白改变,aEEG评分及血清脑红蛋白均可用于晚期早产儿脑损伤的诊断且联合诊断可提高诊断敏感性。展开更多
Previous studies show that chronic acrylamide exposure leads to central and peripheral neu- ropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebr...Previous studies show that chronic acrylamide exposure leads to central and peripheral neu- ropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.展开更多
Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, ...Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the –607C/A （rs1946518） polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 –137G/C （rs187238） polymorphism and the –13T/C （rs11024595） polymorphism in the 5＇-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele （C homozygotes） was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the –13T/C （rs11024595） polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the –607C/A （rs1946518） polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.展开更多
BACKGROUND： Intercellular adhesion molecule-5 （ICAM-5） relieves the damage of beta-amyloid protein to PAJU cells, However, little is known about how ICAM-5 works as a neurotrophic factor, or whether ICAM-5 lessens ...BACKGROUND： Intercellular adhesion molecule-5 （ICAM-5） relieves the damage of beta-amyloid protein to PAJU cells, However, little is known about how ICAM-5 works as a neurotrophic factor, or whether ICAM-5 lessens neuronal damage under ischemic conditions following cerebral infarction. OBJECTIVE： To investigate the effects of ICAM-5 on PAJU cells growth in serum-free medium under ischemic conditions following cerebral infarction. DESIGN, TIME AND SETTING： The cytological in vitro study was performed at the Central Laboratory, Second Xiangya Hospital, Central South University, China, in June 2009. MATERIALS： Human ICAM-5 gene transfected into PAJU-TLN cells was supplied by the Life Science College, Helsinki University, Finland. Empty vector transfected PAJU-NEO cells were established by the Gene Center, Second Xiangya Hospital, Central South University, China. METHODS： PAJU-TLN cells transfected with human ICAM-5 or empty vector were incubated in serum-free medium. MAIN OUTCOME MEASURES： Phase contrast microscopy was used to observe changes in PAJU cell morphology. 3-（4, 5-dimethylthiazolzyl）-2, 5-diphenyltetrazolium bromide was used to determine cell viability. Hoechst 33258 was used to stain cell nuclei. Flow cytometry was utilized to measure the apoptosis rate of both PAJU-TLN and PAJU-NEO cells. RESULTS： Both PAJU-TLN and PAJU-NEO cells were injured by cultivating in serum-free medium, but the survival rate of PAJU-TLN cells was significantly higher. CONCLUSION： ICAM-5 protects PAJU-TLN cells from serum deprivation-induced apoptosis, induces the outgrowth of PAJU cells, and diminishes their morphologic impairment.展开更多
文摘目的探讨振幅整合脑电图(aEEG)评分联合血清脑红蛋白对晚期早产儿脑损伤情况诊断价值。方法回顾性分析2018年1月至2019年12月在邢台市第三医院接受治疗的晚期早产儿133例临床资料。收集患儿aEEG、血清脑红蛋白及早期新生儿神经学评分新生儿20项行为神经测定(NBNA)检测结果。依据判断结果将患者分为脑损伤组(n=45)与无脑损伤组(n=88),比较2组患儿aEEG评分、血清脑红蛋白、NBNA评分,并对aEEG评分、血清脑红蛋白与NBNA评分进行相关性分析。以ROC法判断aEEG评分联合血清脑红蛋白对晚期早产儿脑损伤的诊断价值。结果2组患儿胎龄、性别、分娩方式及出生体质量比较差异无统计学意义(P>0.05)。脑损伤组患儿aEEG评分(7.68±2.04 vs 9.92±3.11)、NBNA评分(33.05±7.14 vs 37.29±2.19)均显著低于无脑损伤组(P<0.01),血清脑红蛋白显著高于无脑损伤组[(158.28±42.09)mg/L vs(119.36±31.84)mg/L,P<0.01]。相关性分析结果显示,aEEG评分与NBNA评分呈显著正相关(r=0.639,P<0.05),血血清脑红蛋白与NBNA评分呈显著负相关关系(r=-0.698,P<0.05)。ROC分析结果显示,aEEG评分对晚期早产儿脑损伤早期诊断cut-off值为10分,AUC为0.893,95%CI为0.830~0.955,敏感度为77.78%,特异性为80.68%;血清脑红蛋白cut-off值为129.71 mg/L,AUC为0.815,95%CI为0.704~0.885,敏感度为73.33%,特异性为84.09%;联合诊断可有效提高诊断敏感度(P<0.05)。结论晚期早产儿脑损伤可引起aEEG评分及血清脑红蛋白改变,aEEG评分及血清脑红蛋白均可用于晚期早产儿脑损伤的诊断且联合诊断可提高诊断敏感性。
基金supported by State Key Development Program for Basic Research of China,No.2012CB525002the National Natural Science Foundation of China,No.30771823
文摘Previous studies show that chronic acrylamide exposure leads to central and peripheral neu- ropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.
文摘Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the –607C/A （rs1946518） polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 –137G/C （rs187238） polymorphism and the –13T/C （rs11024595） polymorphism in the 5＇-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele （C homozygotes） was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the –13T/C （rs11024595） polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the –607C/A （rs1946518） polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.
文摘BACKGROUND： Intercellular adhesion molecule-5 （ICAM-5） relieves the damage of beta-amyloid protein to PAJU cells, However, little is known about how ICAM-5 works as a neurotrophic factor, or whether ICAM-5 lessens neuronal damage under ischemic conditions following cerebral infarction. OBJECTIVE： To investigate the effects of ICAM-5 on PAJU cells growth in serum-free medium under ischemic conditions following cerebral infarction. DESIGN, TIME AND SETTING： The cytological in vitro study was performed at the Central Laboratory, Second Xiangya Hospital, Central South University, China, in June 2009. MATERIALS： Human ICAM-5 gene transfected into PAJU-TLN cells was supplied by the Life Science College, Helsinki University, Finland. Empty vector transfected PAJU-NEO cells were established by the Gene Center, Second Xiangya Hospital, Central South University, China. METHODS： PAJU-TLN cells transfected with human ICAM-5 or empty vector were incubated in serum-free medium. MAIN OUTCOME MEASURES： Phase contrast microscopy was used to observe changes in PAJU cell morphology. 3-（4, 5-dimethylthiazolzyl）-2, 5-diphenyltetrazolium bromide was used to determine cell viability. Hoechst 33258 was used to stain cell nuclei. Flow cytometry was utilized to measure the apoptosis rate of both PAJU-TLN and PAJU-NEO cells. RESULTS： Both PAJU-TLN and PAJU-NEO cells were injured by cultivating in serum-free medium, but the survival rate of PAJU-TLN cells was significantly higher. CONCLUSION： ICAM-5 protects PAJU-TLN cells from serum deprivation-induced apoptosis, induces the outgrowth of PAJU cells, and diminishes their morphologic impairment.
