OBJECTIVETo study the relationship between occupational hazard susceptibility of formaldehyde and genetic polymorphisms of ALDH2 and CYP2E1.

METHODSGenotypes of ALDH2 and CYP2E1 (Rsa I/Pst I site) of 107 subjects exposed to formaldehyde were determined with PCR-RFLP through testing peripheral blood lymphocytes, and the concentration of air formaldehyde in workplace and urine formic acid of the subjects were measured with HPLC. The relationship between genotypes and the urine formic acid increment was analyzed with nonparametric rank sum testing.

RESULTSThe concentration of urine formic acid increment was related with ALDH2 genotypes (chi2 = 9.241, P < 0.05), and the means of urinary formic acid of subjects with GG, GA, AA genotype were (15.84 +/- 6.86), (12.06 +/- 7.94) and (7.31 +/- 5.37) mg/g creatinine, respectively. Mann-Whitney U test showed the formic acid increment between allele G homozygotes and allele A homozygotes was significantly different (U=26, P= 0.033). Our data indicated that the formaldehyde metabolism of ALDH2 GG homozygotic genotype was more active than ALDH2 AA homozygotic genotype(the difference of the two mean rank was 13.30). But the polymorphism of Rsa I / Pst I site of CYP2E1 5'-franking region was not correlated with the concentration of urine formic acid (chi2 = 4.285, P=0.117), and the urinary formic acid means of subjects with C1/C1, C1/C2, C2/C2 genotype were (11.14 +/- 7.91), (12.13 +/- 8.16) and (16.51 -/+ 3.78) mg/g creatinine, respectively. By Stepwise Multiple Regression Analysis, it showed that the urinary formic acid increment might be influenced by FA exposure concentration and ALDH2 genotype, and the model's R2 was 0.196.

CONCLUSIONThe metabolism of formaldehyde in human body was related with the genotypes of ALDH2, but not with the CYP2E1 (Rsa I/Pst I) polymorphisms.

Adolescent ; Adult ; Aldehyde Dehydrogenase ; genetics ; Aldehyde Dehydrogenase, Mitochondrial ; Alleles ; Cytochrome P-450 CYP2E1 ; genetics ; Disease Susceptibility ; Female ; Formaldehyde ; metabolism ; Gene Frequency ; Genotype ; Humans ; Male ; Occupational Exposure ; Polymorphism, Genetic ; Risk Factors

This study was aimed to investigate the effect of baicalin on proliferation and apoptosis of HL-60 cells and its mechanism. Cell proliferation was assayed by using Cell Counting Kit-8. The morphological changes of HL-60 cells were examined by light microscopy and nucleolus morphological changes were observed by fluorescent microscopy after Hoechst 33342 staining. The early cell apoptosis was detected by using flow cytometry with Annexin V-FITC/PI double staining. The expression of caspase-3, caspase-9, Bcl-2 and Bax mRNA was detected by RT-PCR and Western blot assay was carried out to examine Bax, Bcl-2, caspase-8 and cleaved caspase-3 expression. The results showed that Baicalin inhibited the proliferation of HL-60 cells in a time- and concentration-dependent manner. HL-60 cells exhibited typical morphological features (for example, cell shrinkage, membrane blebbing and formation of apoptotic bodies). Cell apoptosis in early stage could be detected, the expression of caspase-3, caspase-9 and Bax mRNA was obviously up-regulated, while the Bcl-2 expression down-regulated, and accordingly Bcl-2/Bax ratio decreased. Such results were consistent with the expression of these proteins. In addition, the expression of cleaved caspase-8 protein was induced significantly after treated with baicalin. It is concluded that baicalin can significantly inhibit the proliferation of HL-60 cells and induce the apoptosis of HL-60 cells, which may occur through decreasing Bcl-2/Bax ratio by intrinsic pathway and through extrinsic pathway. It suggests that baicalin may be a promising drug for the therapy of acute myeloid leukemia.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Proliferation ; drug effects ; Flavonoids ; pharmacology ; HL-60 Cells ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo study the impact of gender factor on the candidate gene study of essential hypertension (EH).

METHODSThe polymerase chain reaction (PCR) was performed to analyze the ACE gene I/D polymorphism of hypertensive patients (50 men and 50 women) and normal controls (50 men and 50 women). The investigation was further focused on possible influence of sex proportion on the conclusion of this kind of research.

RESULTSThe frequency of DD genotype in male hypertensive patients is significantly higher than that in male normal controls (chi(2) = 6.98, P = 0.004). The frequency of D allele in male EH group is significantly higher than that of male normal controls (chi(2) = 6.87, P = 0.009), while no significant difference was observed for II and ID genotype between male EH group and control group (P > 0.05). For female EH group and normal controls, there were no significant differences in frequency of genotype and allele (P > 0.05), the distribution ratio of DD genotype in male EH group is significantly different from that of female EH group (chi(2) = 4.06, P = 0.044). Furthermore, males with DD genotype in EH group had higher SBP and PP than that of males with II and ID genotype (P < 0.05). However, there was no significant difference in DBP in all three genotypes (P > 0.05). At the same time, there was no difference in SBP, DBP and PP (P > 0.05) between II and ID genotype in male EH group. In female hypertensive patients, there was no significant difference in SBP, DBP and PP between all three genotypes (P > 0.05).

CONCLUSIONSThe relationship between DD genotype in male and EH (especially SBP and PP) is closer than any other genotype-EH relationships in both male and female. The gender factor, as a probable confounding factor, can affect many candidate gene studies of essential hypertension including ACE gene I/D polymorphism, and thus biases the conclusion.

Aged ; Female ; Gene Frequency ; Genotype ; Humans ; Hypertension ; genetics ; Male ; Middle Aged ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Genetic ; Sex Factors

OBJECTIVETo study the linkage between K469E polymorphism of intercellular adhesion molecule 1(ICAM1) gene with ICAM1 plasma level and coronary heart disease (CHD) in Han population of China.

METHODSOne hundred and sixty-four controls without CHD and 160 patients with CHD were enrolled in our study. By nested PCR with allele-specific oligonucleotide primers, all patients and controls were genotyped for the ICAM1 polymorphism. And the ICAM1 plasma level was measured by ELISA.

RESULTSIn the patients with CHD, both K allele frequency and the plasma level of ICAM1 were higher than those in control (P<0.05). The individual with K allele had higher plasma level of ICAM1 than that without K allele (344.34+/-128.59 microg/L vs 303.54+/-108.74 microg/L, P=0.008). K allele enhanced the risk of CHD (P<0.01, OR=2.158, 95%CI: 1.250-3.727). There was the K allele cooperation with smoking in influencing the risk of CHD.

CONCLUSIONThere is the polymorphism of ICAM1 K469E gene in Han population of China, and the K allele may be a genetic factor influencing the risk of CHD.

China ; ethnology ; Coronary Disease ; blood ; genetics ; Gene Frequency ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; genetics ; Polymorphism, Genetic ; Potassium ; antagonists & inhibitors

This study was purposed to compare the effect of 3 different cell components for expanding CD4(+) CD25(+) Treg in vitro, and identify their immunosuppressive function. CD4(+) T cells, CD4(+) CD25(-)T cells and CD4(+) CD25(+)T cells were isolated from mouse splenocytes by MACS and then expanded in vitro. Phenotype of the T cell lines and expression of the FOXP3 was determined by flow cytometry. The inhibitory effect of expanded CD4(+) CD25(+) T cells on CD4(+) CD25(-)T cells was tested by MLR method. The results showed that the Treg cells from all the three groups were expanded significantly after culture for 2 weeks. In the CD4(+) T cells group, the proliferation rate was (77.8 ± 5.32) folds with a percentage of Treg cells increasing from (6.61 ± 1.00)% to (15.33 ± 1.31)%. The proliferation rate in the CD4(+) CD25(-) T cells group was (95.20 ± 7.67) folds, with the percentage of CD4(+) CD25(+) T cells raising from (0.37 ± 0.13)% to (9.84 ± 0.98)%. The proliferation rate in the CD4(+) CD25(+) T cells group was (41.20 ± 6.92) folds, the proportion of Treg cells decreased from (86.75 ± 1.25)% to (85.32 ± 1.62)%, and the expression of Foxp3 decreased from (76.92 ± 1.72)% to (75.33 ± 2.11)% during the culture, there were not significant differences in the cell purity and the expression of Foxp3, compared with pre-amplification. The inhibitory test showed that the expanded CD4(+) CD25(+) T cells could inhibit the proliferation of CD4(+) CD25(-) T cells in vitro in a cell dose-dependent manner. It is concluded that the amplification of CD4(+) CD25(+) Treg cells is successful in vitro, especially in the CD4(+) CD25(+) T cells group, the cell purity and Foxp3 gene is not obviously changes after amplification.
Animals ; Cell Proliferation ; Cells, Cultured ; Flow Cytometry ; Forkhead Transcription Factors ; metabolism ; Interleukin-2 Receptor alpha Subunit ; immunology ; Lymphocyte Culture Test, Mixed ; Male ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes, Regulatory ; cytology ; immunology

Adult ; Arteriovenous Malformations ; therapy ; Embolization, Therapeutic ; methods ; Enbucrilate ; therapeutic use ; Female ; Humans ; Kidney ; blood supply ; Male ; Middle Aged

OBJECTIVETo investigate the association of activated coagulation factor VII(F7a) and its gene Msp I polymorphism with coronary heart disease in elderly patients.

METHODSThis was a case-control study, and the method of candidate gene was adopted. F7 genotypes were identified with polymerase chain reaction amplified genomic deoxyribonulieic acid (DNA) and Msp I restriction fragment length polymorphism analysis, and the level of plasma F7a was detected with recombinant tissue factor method for 108 elderly patients with coronary heart disease and 120 sex- and age-matched healthy control subjects.

RESULTS(1) Plasma F7a levels was significantly higher in elderly patients with coronary heart disease than in healthy control subjects (2.88 +/- 0.62 vs 2.58 +/- 0.60 microg/L, P < 0.05), and was significantly higher in old myocardial infarction than in stable angina pectoris (3.12 +/- 0.62 vs 2.76 +/- 0.60, P < 0.05). F7a was shown to be a risk factor for coronary heart disease in elderly patients by Logistic regression analysis (OR=1.21 P < 0.05). (2) The allelic frequencies were in accordance with Hardy-Weinberg equilibrium. The results suggested that the distribution of genotype and allelic frequencies in the groups displayed no significant difference, and there was no difference between the subgroups of coronary heart disease in elderly patients, either (P > 0.05). (3) F7a level was significantly higher in RR genotype than in Q allele carriers (2.72 +/- 0.60 vs 1.98 +/- 0.59 microg/L, P < 0.05) and was associated with F7 gene polymorphism.

CONCLUSIONPlasma F7a level may be an independent risk factor of coronary heart disease in elderly patients, and it may be influenced by the Msp I polymorphism of F7 gene.

Aged ; Binding Sites ; genetics ; Case-Control Studies ; Coronary Disease ; blood ; genetics ; Deoxyribonuclease HpaII ; metabolism ; Factor VII ; genetics ; metabolism ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; genetics ; Genotype ; Humans ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length

OBJECTIVETo explore the distribution of fibrinogen (FGB) B beta polymorphism in Chinese Han population and the association of the polymorphisms with the occurrence of atherosclerotic cerebral infarction (ACI).

METHODSThe B beta gene FGB -455G/A polymorphism was identified by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) in 132 patients with ACI and 148 healthy controls matching on age and sex. Turbidimetric assays were performed to measure the plasma fibrinogen levels of all cases.

RESULTSThe plasma fibrinogen level in ACI group (3.42+/-0.52 g/L), was significantly higher than that in the controls (2.96+/-0.42g/L), P<0.001. The A allele was associated with the elevated plasma fibrinogen levels in both patients and controls. Among the A allele carriers, smokers had significantly higher plasma fibrinogen levels than did the non-smokers (P<0.05). The distribution of B beta gene FGB -455G/A polymorphism was in accordance with the Hardy-Weinberg equilibrium (P>0.05). The A allelic frequency in ACI group (0.258) was significantly higher than that in the control group (0.152) (P<0.05). Logistic regression analysis showed that the cases carrying A allele (GA+AA genotype) had 1.653 times the risk of ACI.

CONCLUSIONThe study demonstrates that A allele of the B beta gene FGB -455G/A polymorphism may be a susceptible predictor of the occurrence of ACI, particularly in smokers.

Aged ; Aged, 80 and over ; Cerebral Infarction ; blood ; genetics ; Female ; Fibrinogen ; genetics ; Humans ; Logistic Models ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Smoking

To approach the effect of CCAAT/enhancer binding proteins (C/EBPs) on un-terminal differentiation of HL-60 cells after treatment with Arsenic Trioxide ( As_2O_3) . Methods The changes of cell morphology were observed by Wright staining, the alteration in the cell proliferation was determined by WST1 experiment and the NBT reduction assay was used to detect the differentiation condition of cells, determination and analysis cell cycle. The expressions of C/EBP? and C/EBP? mRNA in HL-60 cells exposed to ATRA and As_2O_3 were assayed by semi-quantitative RT-PCR. Results It was found that ATRA could up- regulate the mRNA expression of C/EBP? obviously, but down-regulate the mRNA expression of C/EBP?. As_2O_3 could up-regulate the mRNA expression of C/EBP? lightly, down-regulate the expression of C/EBP?. Conclusion Both of ATRA and As_2O_3 can down-regulate the mRNA expression of C/EBP?,but there is no significant difference between these two groups,ATRA and As2O3 can up- regulate the mRNA expression of C/EBP?, with significant differences (P

AIMTo report a series of varicocelectomy performed under pure local anesthesia.

METHODSFrom July 1988 to June 2003, a total of 575 patients, aged between 15 and 73 years, underwent high ligation of the internal spermatic vein for treatment of a varicocele testis under a regional block in which a precise injection of 0.8 % lidocaine solution was delivered to involved tissues after exact anatomical references were made. A 100-mm visual analog scale (VAS) was used to assess whether the pain level was acceptable.

RESULTSThe surgeries were bilateral in 52 cases, and unilateral in 523 cases. All were successfully performed on an outpatient basis except in the case of two patients, who were hospitalized because their surgeries required general anesthesia. Overall, 98.6 % (567/575) of men could go back to work by the end of the first post-operative week and only 8 (1.4 %) men reported feeling physical discomfort on the eighth day. The VAS scores varied from 11 mm to 41 mm with an average of (18.5+/-11.3) mm that was regarded as tolerable.

CONCLUSIONThis study has shown varicocelectomy under local anesthesia to be possible, simple, effective, reliable and reproducible, and a safe method with minimal complications. It offers the advantages of more privacy, lower morbidity, with no notable adverse effects resulting from anesthesia, and a more rapid return to regular physical activity with minor complications.

Acetaminophen ; administration & dosage ; Adolescent ; Adult ; Aged ; Analgesics, Non-Narcotic ; administration & dosage ; Anesthesia, Local ; Anesthetics, Local ; administration & dosage ; Follow-Up Studies ; Humans ; Lidocaine ; administration & dosage ; Male ; Middle Aged ; Outpatients ; Pain, Postoperative ; drug therapy ; Postoperative Complications ; Varicocele ; surgery ; Vascular Surgical Procedures ; methods