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Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 05/2012; 28(3):218-20.
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ABSTRACT: Adipose-derived stromal cell (ADSC) differentiation into neural cells in vitro is becoming widely studied. However, there are few reports on astrocytes following differentiation, and particularly on maturation and electrophysiology. In this study, we used various methods to determine ADSC-derived astrocyte maturity.
Chemical induction with isobutylmethylxanthine (IBMX) was used to differentiate adult ADSCs into astrocytes followed by hematoxylin-eosin (HE) staining to observe morphology and transmission electron microscopy for cellular ultrastructure assessment. Immunofluorescence was used to detect expression of neural stem cell marker nestin as well as glial markers glial fibrillary acidic protein (GFAP) and S-100. In addition, we measured membrane potentials in bis-(1,3-dibarbituric acid) trimethine oxanol-labeled ADSCs and astrocytes by stimulation with a high potassium solution under an inverted fluorescence microscope. Finally, cell cycle distribution was detected by flow cytometry.
Typical astrocyte morphology was shown by HE staining after 48-hour differentiation. Glial fibril was observed with transmission electron microscopy. GFAP and S-100 were not expressed in the control group, but were expressed within 24-hour differentiation and reached a maximum at day 14 with no change up to day 28. Nestin was weakly expressed in control cells and also reached a maximum at day 14 with the percentage of positive cells constant until day 21 followed by a decrease. Differentiated cell membrane potentials after stimulation with potassium were slightly increased, and then gradually declined over time. There was no significant membrane potential change in the control group. Flow cytometry showed that the percentage of cells in G0/G1 phase was 93% and only 5% in S phase.
ADSCs were differentiated into mature astrocytes with typical characteristics including morphology, ultrastructure, marker protein expression, mature potassium channels and mitotic capacity.
Chinese medical journal 09/2011; 124(17):2656-60. · 0.86 Impact Factor
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ABSTRACT: The morbidity and mortality of prostate cancer have been increasing rapidly in recent China. There were few studies investigating prostate-specific antigen (PSA) values ranges in the healthy Chinese population. We performed this study to determine the distribution of serum PSA in a large healthy Chinese population.
From January 2001 to May 2008, 11 150 healthy Chinese men aged 30 - 79 years came to our hospital for routine health check-up. All subjects without a previous diagnosis of prostate cancer, a history of prostate surgery, or urogenital tract infection were proposed to undergo systematic serum PSA measurement and digital rectal examination (DRE). Men with normal DRE and PSA ≤ 4.0 ng/ml and those PSA > 4.0 ng/ml or abnormal DRE but without adverse findings on prostate biopsy were included (n = 9358). Age and serum PSA concentration were recorded and correlated through Logistic regression analysis.
The 95th percentile serum PSA concentration was 1.89 ng/ml for men aged 30 to 39 years, 2.19 ng/ml for men aged 40 to 49 years, 2.88 ng/ml for men aged 50 to 59 years, 4.42 ng/ml for men aged 60 to 69 years, and 6.52 ng/ml for men aged 70 to 79 years. The serum PSA concentration correlated with age (P < 0.0001) with an annual increase of 0.97% for men in 40 years, 1.58% for men in 50 years, 3.04% for men in 60 years, and 3.99% for men in 70 years.
The serum PSA level correlates directly with age in Chinese men older than 40 years, not in Chinese men younger than 40 years old. Chinese men have lower PSA level compared with white men above 60 years of age, not in those under 60 years of age.
Chinese medical journal 04/2011; 124(8):1189-92. · 0.86 Impact Factor
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ABSTRACT: To study the distribution characteristics of Beta-fibrinogen (Fg)B gene-854G/A, -455G/A, -249C/T, -148C/T, 448G/A and Bcl-1 G/A polymorphism in North China Han population, and the influence on plasma Fg concentration and molecular reactivity. Further more, to explore the role of Fg gene polymorphisms combining with multi-physiological and environmental factors in the development of cerebral infarction.
Cluster sampling, health examination and questionnaires surveys of 1652 subjects from Tangshan Kailuan Group Corporation were conducted. Blood biochemistry, Fg concentration, fibrin monomer polymerized velocity (FMPV), absorbance maximum (Amax) and FMPV/Amax were measured. The six polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism.
In the population, the proportion of the FgB beta-249 T variation allele was 65.49%, while the proportion of the rest loci was predominantly wild type. The significant differences in Fg concentration and FMPV/Amax were found in -854 genotype groups. The Fg concentration in -854GA group was higher than those in GG and AA group. Only the distribution frequencies of FgB beta Bcl-1 A variation allele, GA and AA genotype in the cerebral infarction group were higher than those in non-infarction group, and the prevalence of cerebral infarction in AA genotype group was higher than other groups (the probability value of above-mentioned results were all P<0.01).
FgB beta Bcl-1A allele and variation genotype were susceptible to cerebral infarction. FgB beta-455GA/448G linkage genotype may contribute to the increased plasma Fg concentration. FgB beta-854 was one of the main controlling gene loci for plasma Fg concentration and molecular reactivity.
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 09/2009; 30(9):582-7.
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ABSTRACT: To study the association of beta-fibrinogen(Fg) gene -148 C/T and 448 G/A polymorphisms, plasma Fg concentration, molecular reactivity and the type of cerebral infarction.
Gene polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism. The plasma Fg concentration and the molecular reactivity were also determined.
The Fg concentration in MCI patients with T -148 allele was higher than that in PCI patients and controls. The MCI patients with A448 allele had higher Fg concentration, FMPV and FMPV/Amax when compared with controls, and had higher FMPV/Amax when compared with PCI patients.
FgB beta -148 and 448 mutational genotypes have impact on Fg concentrationì and therefore increase the risk of MCI.
Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 11/2005; 22(5):572-4.
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ABSTRACT: To explore the relation of angiotensin-converting enzyme (ACE) gene polymorphism, angiotensin II type I receptor (ATIR) gene polymorphism and other factors on cerebral infarction.
One thousand three hundred fifty-one subjects from Tangshan coalmine were enrolled with study method of cluster sampling. Face to face interviews were conducted to fill in questionnaires by trained interviewers. ACE gene, ATIR gene and inflammation factors including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-8, IL-10, C reactive protein (CRP), fibrinogen (Fg), fibrin monome polymerized velocity (FMPV), absorbance maximum (A(max)), FMPV/A(max), were measured.
No different prevalence rates of ACE genotype were found on cerebral infarction. The distributions of AA genotype of ATIR gene in the cerebral infarction was higher than that of the controls. The prevalence of AA genotype was higher than other groups, but the prevalence of combined genotype did not show much difference. Under the existence of factors that related to cerebral infarction, AA genotype frequencies were higher than those of non-smoking and with hypertension. IL-6, ATIR gene polymorphism, sex, FMPV/A(max) were strongly related to cerebral infarction. The level of IL-6 was higher than the normal ones.
The prevalence of cerebral infarction obviously increased in the hypertensive groups having AA genotype of ATIR gene. In the cerebral infarction groups, the level of IL-6 was higher than that in the normal population, indicating that these can be resulted from local inflammation and immunity reactivity. Environmental and genetic factors in the pathogenesis of cerebral infarction might have coordinating functions.
Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 10/2003; 24(9):822-6.
