脂联素受体2基因+33371Gln/Arg、细胞色素P4502E1 基因RsaⅠ位点多态性和吸烟与非酒精性脂肪性肝病的相关性

目的探讨脂联素受体2（AdipoR2）基因+33371Gln/Arg、细胞色素P4502E1（CYP2E1）基因RsaⅠ位点多态性和吸烟与非
酒精性脂肪性肝病（nonalcoholic fatty liver disease, NAFLD）发病之间的关系。方法采用病例-对照研究的方法,以750例NAFLD
患者及750例健康对照者的外周血白细胞为样本,利用聚合酶链反应（polymerase chain reaction, PCR）技术分析了+33371Gln/
Arg和CYP2E1-RsaⅠ基因多态性。结果+33371Gln/Arg（A/A）基因型和CYP2E1-RsaⅠ（c2/c2）基因型频率分布分别为39.20%、
71.73%（病例组）和21.07%、43.07%（对照组）。+33371Gln/Arg（A/A）患NAFLD的风险显著增加（OR=2.4156,95% CI=1.8164~
4.0725）。CYP2E1-RsaⅠ（c2/c2）基因型者患NAFLD的风险也显著增加（OR=3.3547,95% CI=1.9182~4. 5057）。+33371Gln/
Arg（A/A）/CYP2E1-RsaⅠ（c2/c2）基因型者在NAFLD 组和对照组中的分布频率分别为32.67%和6.40%。+33371Gln/
Arg（A/A）/CYP2E1-RsaⅠ（c2/c2）基因型者患NAFLD的风险显著增加（OR=9.9264,95% CI=4.2928~12.4241）。病例组的吸烟
率显著高于对照组的吸烟率（OR=2.5919,95% CI=1.4194~4.9528）,+33371Gln/Arg（A/A）/CYP2E1-RsaⅠ（c2/c2）基因型与吸烟
有协同作用（OR=34.6764,95% CI=18.9076~61.5825）。结论+33371Gln/Arg（A/A）/CYP2E1-RsaⅠ（c2/c2）基因型和吸烟是
NAFLD的易患因素,三者的联合在NAFLD的发生中起着协同的作用。
     

Heme oxygenase-1 promotes Caco-2 cell proliferation and migration by targeting CTNND1

Background Heme oxygenase-1 （HO-1） can be induced by inflammatory cytokines,oxidation,ischemia,hypoxia,and endotoxins.As a ＂graft survival protective gene,＂ HO-1 is a hot spot in organ transplantation research.However,the role of HO-1 gene expression in the function of human colon adenocarcinoma cell line （Caco-2） cells has not been reported previously.Methods The role of HO-1 in the proliferation and migration of Caco-2 cells was analyzed using a stable HO-1 expression plasmid.We constructed a recombinant adeno-associated virus plasmid containing the HO-1 gene,heme oxygenase 1 （HMOX1）,which was transfected into Caco-2 intestinal cells.We identified a number of target genes by global microarray analysis combined with real-time polymerase chain reaction （PCR） and chromatin immunoprecipitation assay.Results Our results showed that significant HO-1 upregulation was demonstrated in the Caco-2 cells after HO-1 transfection.Restoration of HO-1 expression promoted proliferation and invasion in vitro.The CTNND1 gene,a member of the armadillo protein family,was identified as a direct HO-1 target gene.Conclusion Overexpression of HO-1 promotes Caco-2 cell proliferation and migration by targeting the CTNND1 gene.     

消积饮通过Akt 信号可对人肺癌A549细胞株产生抑制增生及促进凋亡作用

Objective:To investigate the inhibitive effect and the underlying mechanism of Xiaoji Decoction(消积饮,XJD)in human lung cancer A549 cells.Methods:A549 cells in logarithmic proliferation were cultivated in RPMI-1640 containing 10%low,medium or high dosages of XJD serum.The inhibitive effect of XJD in A549 cell proliferation was assessed by methylthiazolyldiphenyl-tetrazolium bromide(MTT)assay.The pro-apoptotic effect of XJD in A549 cells was observed by fluorescence microscope via Hoechst 33258 staining.The role of the Akt signaling pathway was observed by examining the presence of p-Akt protein by Western blot and the mRNA expression of downstream proteins such as Bcl-2/Bcl-XL-associated death promoter(BAD)and caspase-9 by real time polymerase chain reaction.Results:MTT assay revealed that XJD could inhibit A549 proliferation in a dose-and time-dependent manner.Hoechst 33258 staining showed that XJD induced the typical nuclear apoptotic morphology after XJD treatment.Moreover,XJD could reduce the phosphorylation of Akt and increase the mRNA expression of BAD and caspase-9.Conclasions:XJD can inhibit the proliferation of A549 cells in a dose-and time-dependent manner through signaling Akt pathway via up-regulating the expression of BAD and caspase-9.XJD may provide a novel therapeutic model for lung cancer and deserve further study.     

The remedial effect of soluble interleukin-1 receptor type Ⅱ on endometriosis in the nude mouse model

Objective： Recent studies have shown that the local expression of soluble interleukin （IL） -1 receptor type Ⅱ （slL-1 R Ⅱ ） in endometrial tissue of women with endometriosis is decreased, and the depression of IL-1 R Ⅱ was more significant in infertile women than that in fertile women with endometriosis. In this research, we investigated the remedial effect of slL-1-R Ⅱ administration on endometriosis in the nude mouse model. Methods： Nineteen nude model mice with endometriosis were randomly divided into three groups： group A was treated by intraperitoneal administration with only slL-1 R Ⅱ for two weeks, group B was similarly treated with only IL- 1, and group C （control） was administered saline. After 2 weeks, the size of the ectopic endometrial lesions was calculated, and the expression of vascular endothelial growth factor （VEGF） and B-cell lymphoma leukemia-2 （Bcl- 2） were detected by immunohistochemistry. The IL-8 and VEGF levels in the peritoneal fluid （PF） and serum were also measured by enzyme-linked immunosorbent assay （ELISA）. Results： The mean size of ectopic endometrial lesion did not differ between the three groups （P 〉 0.05）. Compared with the control, the expression of VEGF and Bcl-2 was significantly lower in group A, and higher in group B. In the three groups, the levels of IL-8 in the PF and serum were highest in group A, and lowest in group B. Conclusion： slL-1 R Ⅱ may suppresse hyperplasia of ectopic endometriosis, perhaps by reducing the expression of certain cytokines, such as VEGF, IL-8, and Bcl-2, which could provide a new clinical strategy for the treatment of endometriosis.     

The cardioprotection induced by lipopolysaccharide involves phos- phoinositide 3-kinase/Akt and high mobility group box 1 pathways

Objective： The mechanisms by which lipopolysaccharide （LPS） pretreatment induces cardioprotection following ischaemia/reperfusion （I/R） have not been fully elucidated. We hypothesized that activation of phosphoinositide 3-kinase （PI3K）/Akt and high mobility group box 1 （HMGBxl） signaling plays an important role in LPS-induced cardioprotection. Methods： In in vivo experiments, age- and weight- matched male C57BL/10Sc wild type mice were pretreated with LPS before ligation of the left anterior descending coronary followed by reperfusion. Infarction size was examined by triphenyltetrazolium chloride （TTC） staining. Akt, phospho-Akt, and HMGBxl were assessed by immunoblotting with appropriate primary antibodies. In situ cardiac myocyte apop- tosis was examined by the TdT-mediated dUTP nick-end labeling （TUNEL） assay. In an in vitro study, rat cardiac myoblasts （H9c2） were subdivided into two groups, and only one was pretreated with LPS. After pretreatment, the cells were transferred into a hypoxic chamber under 0.5% 02. Levels of HMGBxl were assessed by immunoblot. Results： In the in vivo experiment, pretreatment with LPS reduced the at risk infarct size by 70.6% and the left ventricle infarct size by 64.93% respectively. Pretreatment with LPS also reduced cardiac myocytes apoptosis by 39.1% after ischemia and reperfusion. The mechanisms of LPS induced cardioprotection involved increasing PI3K/Akt activity and decreasing expression of HMGBxl. In the in vitro study, pretreatment with LPS reduced the level of HMGBxl in H9c2 cell cytoplasm following hypoxia. Conclusion： The results suggest that the cardioprotection following I/R induced by LPS pretreatment involves PI3K/Akt and HMGBxl pathways.     

Expression of human hepatic lipase negatively impacts apolipoprotein A-Ⅰ production in primary hepatocytes from Lipc-null mice

This study aimed to examine whether expression of human hepatic lipase（hHL） exerted an intracellular effect on hepatic production of apolipoprotein（apo） A-I.The levels of secreted and cell-associated apoA-I were contrasted between primary hepatocytes isolated from Lipc-nuW and C57BL/6 mice,and between Lipc-nuW hepatocytes transfected with either hHL-encoding or control adenovirus.An HSPG-binding deficient hHL protein（hHLmt） was used to determine the impact of cell surface binding on HL action.Accumulation of apoA-I in conditioned media of primary hepatocytes isolated from Lipc-nuW mice was increased as compared to that from C57BL/6 mice.Metabolic labeling experiments showed that secretion of ＇＇S-apoA-I from Lipc-nuW cells was significantly higher than that from C57BL/6 cells.Expression of hHL in Lipc-nuW hepatocytes,through adenovirus-mediated gene transfer,resulted in decreased synthesis and secretion of ＇S-apoA-I,but not S-apoE,as compared with cells transfected with control adenovirus.Expression of HSPG-binding deficient hHLmt in Lipc-nuW cells also exerted an inhibitory effect on apoA-I production,even though hHLmt displayed impaired exit from the endoplasmic reticulum as compared with hHL.Subcellular fractionation revealed that expression of hHL or hHLmt led to increased microsome-association of apoA-I relative to non-transfected control.Expression of hHL negatively impacts hepatic production of apoA-I.     

Over-expression of heme oxygenase-1 in peripheral blood predicts the progression and relapse risk of chronic myeloid leukemia

Background There are limited eligible clinical markers at present to monitor the progress of chronic myeloid leukemia （CML）.Heme oxygenase-1 （HO-1）,as one of the most important oxidation-regulating enzymes in vivo,suggests the onset and progression of cancer when highly expressed.Furthermore,HO-1 level is related with the occurrence and development of hematological diseases.But the relationship between HO-1 expression and progression/relapse of CML has seldom been studied hitherto.This study aimed to investigate the relationship between them to find out a new molecular marker for prediction.Methods A total of 60 peripheral blood and bone marrow （BM） samples from 25 CML patients in different phases were collected respectively to detect the expressions of HO-1 and bcr/abl using real-time PCR.Routine blood test was performed to detect the changes of leukocyte and platelet counts.The proportion of primitive cells in BM was detected by flow cytometry.The relationship between high HO-1 expression and CML progression and relapse was explored by the analysis of variance by Wilcoxon test and linear regression analysis.The diagnostic accuracy and cutoff values were determined by receiver operating characteristic curve.Results Relative expression of HO-1 mRNA in CML patients peripheral blood was significantly higher than that of donors （P 〈0.0001）,which were 0.57±3.78 and （1.417±1.125）×10-6,respectively.HO-1 expression level in CML patients was 0.061 5±0.062 4,which decreased to 0.009 4±0.006 7 upon CMoR,and remained remarkably higher 0.016 3±0.017 5 than that of normal donors （1.417±1.125）× 10-6,P 〈0.001.When relapse occurred,HO-1 expression significantly increased from 0.020 6±0.021 0 to 3.852±10.285 in CMoR stage and undergoing relapse.According to progression of CML,HO-1 expression level in CML patients increased from CP （0.009 5±0.017 6） to AP （0.028 0±0.055 7） and then to BP （0.276 7± 0.447 0）.And there was a linear correlation between HO-1 expression and proportion     

Hyperbaric oxygen intervention on expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in spinal cord injury models in rats

Background Hyperbaric oxygen （HBO） intervention is a main therapeutic method and the curative effect has been certified for spinal cord injury （SCI）, but the mechanisms of the neuroprotective effect of HBO on SCI remain elusive. This study aimed to observe the change in expression of hypoxia-inducible factor-1α （HIF-1α） and vascular endothelial growth factor （VEGF） after SCI at different time points and to investigate the neuroprotective mechanism of HBO on SCI in rats.     

A genetic variant in pseudogene E2F3P1 contributes to prognosis of hepatocellular carcinoma

Certain pseudogenes may regulate their protein-coding cousins by competing for miRNAs and play an active biological role in cancer. However, few studies have focused on the association of genetic variations in pseudogenes with cancer prognosis. We selected six potentially functional single nucleotide polymorphisms （SNPs） in cancerrelated pseudogenes, and performed a case-only study to assess the association between those SNPs and the prognosis of hepatocellular carcinoma （HCC） in 331 HBV-positive HCC patients without surgical treatment. Log-rank test and Cox proportional hazard models were used for survival analysis. We found that the A allele of rs9909601 in E2F3P1 was significantly associated with a better prognosis compared with the G allele [adjusted hazard ratio （HR） = 0.69, 95% confidence interval （CI） = 0.56-0.86, P = 0.001]. Additionally, this protective effect was more predominant for patients without chemotherapy and transcatheter hepatic arterial chemoembolization （TACE） treatment. Interestingly, we also detected a statistically significant multiplicative interaction between genotypes of rs9909601 and chemotherapy or TACE status on HCC survival （P for multiplicative interaction 〈 0.001）. These findings indicate that rs9909601 in the pseudogene E2F3P1 may be a genetic marker for HCC prognosis in Chinese.     

Effects of suppressed autophagy on mitochondrial dynamics and cell cycle of N2a cells

Autophagy dysregulation, mitochondrial dynamic abnormality and cell cycle re-entry are implicated in the vulnerable neurons of patients with Alzheimer＇s disease. This study was designed to testify the association among autophagy, mitochondrial dynamics and cell cycle in dividing neuroblas- toma （N2a） cells. The N2a cells were cultured in vitro and treated with different concentrations of 3-methyladenine （3-MA）. The cell viability was detected by methyl thiazolyl tetrazolium （MTT） assay. They were randomly divided into control group （cells cultured in normal culture medium） and 3-MA group （cells treated with 10 mmol/L 3-MA）. The cell cycle was analyzed in the two groups 3, 6, 12, and 24 h after treatment by flow cytometry. Western blotting was used to evaluate the expression levels of mitofission 1 （Fisl）, mitofusin 2 （Mfn2）, microtubule-associated protein 1 light chain 3 （LC3）, cell cy- cle-dependent kinase 4 （CDK4） and cdc2. The flow cytometry revealed that the proportion of cells in G2/IVI was significantly increased, and that in G0/G1 was significantly reduced in the 3-MA group as compared with the control group. Western blotting showed that the expression levels of Fisl, LC3, and CDK4 were significantly up-regulated in the 3-MA group at the four indicated time points as compared with the control group. Mfn2 was initially decreased in the 3-MA group, and then significantly in- creased at 6 h or 12 h. Cdc2 was significantly increased in the 3-MA group at 3 h and 6 h, and then dropped significantly at 12 h and 24 h. Our data indicated that 3-MA-induced suppressed autophagy may interfere with the cell cycle progression and mitochondrial dynamics, and cause cell death. There are interactions among cell cycle, mitochondrial dynamics and autophagy in neurons.     

Upregulated heme oxygenase-1 expression of mouse mesenchymal stem cells resists to chemotherapy-induced bone marrow suppression

Background Bone marrow hematopoietic function suppression is one of the most common side effects of chemotherapy.After chemotherapy,the bone marrow structure gets destroyed and the cells died,which might cause the hematopoietic function suppression.Heme oxygenase-1 （HO-1） is a key enzyme of antioxidative metabolism that associates with cell proliferation and resistance to apoptosis.The aim of this study was to restore or resist the bone marrow from the damage of chemotherapy by the HO-1 expression of mouse mesenchymal stem cells （mMSCs） homing to the mice which had the chemotherapy-induced bone marrow suppression.Methods One hundred and sixty female Balb/c mice （6-8-weeks old） were randomly divided into four groups.Each group was performed in 40 mice.The control group was intraperitoneally injected for 5 days and tail intravenously injected on the 6th day with normal saline.The chemotherapy-induced bone marrow suppression was established by intraperitoneally injecting cyclophosphamide （CTX） into the mice which performed as the chemotherapy group.The mMSCs were tail intravenously injected into 40 chemotherapically damaged mice which served as the mMSCs group.The difference between the HO-1 group and the mMSCs group was the injected cells.The HO-1 group was tail intravenously injected into the mMSCs that highly expressed HO-1 which was stimulated by hemin.The expression of HO-1 was analyzed by Western blotting and RT-PCR.Cell proliferation was measured using the 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay.Histopathologic examinations were performed 1 week after injection.Results Compared with the control group,the expression levels of HO-1 mRNA and protein were significantly higher in the HO-1 group （all P ＜0.05）,even obviously than the mMSCs group.CTX treatment induced apoptosis and inhibited proliferation.After injected,the white blood cell （WBC）,red blood cell （RBC） and platelet （PLT） declined fast and down to the bottom at the 7th day.The bone marrow structure was destroyed incomplete.In vitro,the survival rate of cells in chemotherapy group was less than 50％ after 24 hours.In contrast,mMSCs could do a favor to the cellular cleavage and proliferation.They slowed down the cell mortality and more than 50％ cells survived after 24 hours.The effects of blocking apoptosis and bone marrow recovery could be more effective in the HO-1 group.In the HO-1 group,it had observed that the bone marrow structure became complete and the hemogram closed to normal at 7th day.Conclusions HO-1 played an important role in promoting the recovery of CTX-induced hematopoietic damage.We suclgest that HO-1 is able to restore the functions of chemotherapy-induced hematopoietic damage.     

Expression of ectonucleotide pyrophosphatase-1 in end-plate chondrocytes with transforming growth factor beta 1 siRNA interference by cyclic mechanical tension

Background Ectonucleotide pyrophosphatase/phosphodiesterase （ENPP）-I is a membrane-bound protein that catalyzes the hydrolysis of extracellular nucleoside triphosphates to monophosphate and extracellular inorganic pyrophosphate （ePPi）. Mechanical stimulation regulates ENPP-1 expression. This study sought to investigate the changes in ENPP-1 expression after stimulation using cyclic mechanical tension （CMT）.     

P1 gene of Mycoplasma pneumoniae in clinical isolates collected in Beijing in 2010 and relationship between genotyping and macrolide resistance

Background Mycoplasma pneumoniae is a common pathogen that caused community-acquired pneumonia （CAP）. P1 protein served as major adhesion and immunodominant protein in Mycoplasma pneumoniae, but little about P1 gene was learned and the relationship between P1 genotype and macrolide resistance has yet to be explored.     

不同中医证候患者接受骨髓血管再生术治疗的表现与再生障碍性贫血临床病理特征联系

Objective： To explore differences in bone marrow angiogenesis seen in aplastic anemia （AA） patients presenting with differential Chinese medicine （CM） syndrome, and to correlate these differences with clinical pathology. Methods： Thirty-five patients were enrolled, including 18 with ＂yang deficiency syndrome＂ and 17 with ＂yin deficiency syndrome.＂ Bone marrow biopsies and serum were collected. Microvessel density （MVD） and positive expression of vascular endothelial-derived growth factor （VEGF） were detected by immunohistochemisty. Hypoxia inducible factor -α （HIF-α ）, and VEGF expression were assayed by enzyme-linked immunoabsorbent assay （ELISA）, serum lactate dehydrogenase （LDH） was tested by enzyme method and liquid chip technology was used to detected the expression of interleukin （IL）-2, IL-4, IL-6, IL-10, interferon （IFN）-＇y and tumor necrosis factor （TNF）-α. Results： Counts for leukocytes, absolute neutrophils and platelets in ＂yin deficiency syndrome＂ were lower than those found in ＂yang deficiency syndrome＂ （P〈0.05）. MVD and VEGF expression, and the positive rate of CD34 and VEGF in bone marrow were lower in hA, especially in ＂yin deficiency syndrome＂ （P〈0.01 or P〈0.05）. ＂Yin deficiency syndrome＂ displayed decreased VEGF and LDH expression, and enhanced expression of HIF-α as compared to ＂yang deficiency syndrome＂ （P〈0.05）. Levels of IL-4 and IL-6 were higher in AA （P〈0.01）, but IL-10 was decreased （P〈0.05）. High TNF-c~ expression was seen in ＂yang deficiency syndrome＂ and IFN- γ expression was decreased in ＂yin deficiency syndrome＂ as compared with normals （P〈0.01 and P〈0.05, respectively）. Conclusion： AA patients have lower MVD than normals, especially in ＂yin deficiency syndrome.＂ MVD might differentially correlate to disease severity, and could be dependent on bone marrow or serum VEGF expression and LDH. Additionally, IL-2, IL-10, IL-4 and IFN- γ were negatively associated while IL-6 and TNF- α were positively associated with MVD.     

Relationships among magnetic resonance imaging, histological findings, and IGF-I in steroid-induced osteonecrosis of the femoral head in rabbits

Objective： To study the relationships among magnetic resonance imaging （MRI）, histological findings, and insulin-like growth factor-Ⅰ （IGF-Ⅰ） in steroid-induced osteonecrosis of the femoral head in rabbits. Methods： Thirty rabbits were randomly divided into experimental Group A （n= 15） and control Group B （n= 15）. The 7.5 mg/kg （2 ml） of dexamethasone （DEX） and physiological saline （2 ml） were injected into the right gluteus medius muscle twice at one-week intervals in animals of Groups A and B, respectively. At 4, 8 and 16 weeks after obtaining an MRI, the rabbits were sacrificed and the femoral head from one side was removed for histological study of lacunae empty of osteocytes, subchondral vessels, and size of fat cells under microscopy, and the femoral head from the other side was removed for enzyme-linked immunoadsorbent assay （ELISA） for IGF-Ⅰ. Results： At 4, 8 and 16 weeks after treatment, no necrotic lesions were detected in Group B, while they were detected in Group A. Light microscopy revealed that the fat cells of the marrow cavity were enlarged, subchondral vessels were evidently decreased, and empty bone lacunae were clearly increased. The IGF-Ⅰ levels in Group A were significantly higher than those in Group B. At 8 weeks after the DEX injection, the MRI of all 20 femora showed an inhomogeneous, low signal intensity area in the femoral head, and at 16 weeks, the findings of all 10 femora showed a specific ＂line-like sign＂. The MRI findings of all femora in Group B were normal. Conclusion： MRI is a highly sensitive means of diagnosing early experimental osteonecrosis of the femoral head. However, the abnormal marrow tissues appeared later than 4 weeks when the expression of IGF-Ⅰ increased. This reparative factor has an early and important role in response to steroid-induced osteonecrosis of the femoral head, and provides a theoretical foundation for understanding the pathology and designing new therapies.     

Association oftransforming growth factor-β1 gene variants with risk of coal workers'pneumoconiosis

Objective： The aim of this case-control study was to explore whether five tagging single nucleotide poly- morphisms （tSNPs） within the transforming growth factor-ill （TGF-fll） gene were involved in manifestation of inflammatory and fibrotic processes associated with coal workers pneumoconiosis （CWP）. Methods： The study included 508 CWP patients and 526 controls who were underground coal miners from Xuzhou Mining Business Group. Five tSNPs were selected from the HapMap and detected by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） method. Results： The single SNP analysis showed that the genotype frequencies of SNP2 （rs1800470, ＋869T/C, extron 1） and SNP5 （rs11466345, intron 5） in CWP cases were significantly different from those in controls. Multivariate logistic regression analysis revealed that SNP2 （rs1800470） CC genotype was associated with decreased risk of CWP （OR = 0.50, 95% CI = 0.32-0.78）, which was evident among subgroups of those never smoke （OR = 0.40, 95%CI = 0.24-0.66）, cases with stage Ⅱ（OR = 0.41, 95%CI = 0.22-0.76） and exposure period （〈 28 y： OR = 0.54, 95%CI = 0.31-0.95; ≥ 28 y： OR = 0.52, 95%CI = 0.32-0.96）. However, the SNP5 （rs11466345） GG genotype was associated with an increased risk of CWP （OR = 2.5, 95%CI = 1.36-4.57）, and further stratification analysis showed that the risk of CWP was increased in both smoking and nonsmoking groups, shorter and longer exposure groups, while the risk of CWP was only increased in patients with stage I and Ⅱ. Conclusion： This study suggests that TGF-β1 polymorphisms may contribute to susceptibility of CWP.     

Thyroid Examination in Low-Radiation Exposed Iraqi Clean-up Workersmlmmunogenetic Study

Aim： Twenty nine Iraqi cleanup workers at A1-Tuwaitha Research site were examined for the prevalence of thyroid disorders. Materials and Methods： Serological evidence were carried out by measuring the levels of triiodothyronine （T3）, thyroxin （T4）, thyroid stimulating hormone （TSH） and anti-thyroglobulin （anti-Tg）, anti-thyroperoxidase （anti-TPO） auto antibodies. Genotyping for HLA-DRB1 and HLA-DQB1 alleles was done by using the molecular biological technique of polymerase chain reaction-sequence specific oligonucleotide （PCR-SSO）. Results： The hormonal study revealed that T4 and T3 levels were below the normal range in five and four workers respectively, TSH was below the normal range in two （7%） workers and elevated in the other three workers （10%）. Anti-TPO and anti-Tg antibodies were also determined. The results were positive in 24% and 17% of cleanup workers respectively. Comparison between 16 cleanup workers group A （risk-group）, 13 group B （exposed） and 30 （non exposed） control showed that HLA-DQBI＊06 allele was significantly P = radiation was most prominent in HLA-DQB 1＊03, P = 0.4 when age-dependent heterogeneity in response to low doses of radiation be involved in decreased thyroid disorder risk. 0.01 lower among group A than controls group. Risk elevation by compared with exposed control. Conclusion： Our data suggest an and the immunogenetic marker such as HLA- DQB 1＊06 allele may     

Antigen presenting cells may be able to distinguish between normal and radiatedSchistosoma japonicum cercaria:anin vitro observation

Objective： To observe the discrepancies of responses induced by Schistosoma japonicum （S. japonicum） normal cercaria antigen （NCA） and ultraviolet （UV） -radiation-attenuated cercaria antigen （UVACA） in an in vitro system. Methods： S. japonicum cercariae were collected and UVACA and NCA were prepared. Mouse macro- phage model cells （RAW 264.7） were treated with medium, NCA （40 μg/mL） or UVACA （40 μg/mL） in the presence or absence of recombinant mouse interferon gamma （rmIFN-γ; 4 ng/mL） for 48 h. Cell surface staining and flow cytometry were used to assess the major histocompatibility complex （MHC） Ⅱ expression, and data were expressed as mean fluorescence intensities （MFI）. Interleukin （IL） -10, IL-6 and prostaglandin E2 （PGE2） in cell culture supernatant were evaluated by commercial enzyme-linked immunosorbent assays. Results： NCA significantly suppressed IFN-7-induced MHC Ⅱ expression on RAW 264.7 cells. In the presence of 1FN-7, NCA significantly promoted IL-6, IL-10 and PGE2 secretion from RAW 264.7 cells. In the presence of IFN-γ, UVACA significantly promoted IL-10 but not IL-6 and PGE2 secretion from RAW 264.7 cells and showed no effect on IFN-γ-induced MHC Ⅱ expression. Compared with UVACA, NCA significantly suppressed IFN-γ-induced MHC Ⅱ expression and significantly promoted IL-6, PGE2 and IL-10 secretion from RAW 264.7 cells. Conclusion： RAW 264.7 cells respond differently to NCA and UVACA. NCA can significantly suppress IFN-γ-induced MHC Ⅱ expression and significantly promote IL-6, IL-10 and PGE2 secretion from RAW 264.7 cells compared with UVACA.     

Availability and toxicity of Fe（Ⅱ） and Fe（Ⅲ） in Caco-2 cells

The objective of the present study was to compare the toxicity and availability of Fe（Ⅱ） and Fe（Ⅲ） to Caco-2 cells. Cellular damage was studied by measuring cell proliferation and lactate dehydrogenase （LDH） release. The activities of two major antioxidative enzymes [superoxide dismutase （SOD） and glutathione peroxidase （GPx）] and differentiation marker （alkaline phosphatase） were determined after the cells were exposed to different levels of iron salts. The cellular iron concentration was investigated to evaluate iron bioavailability. The results show that iron uptake of the cells treated with Fe（I1） is significantly higher than that of the cells treated with Fe（Ⅲ） （P〈0.05）. Fe（Ⅱ） at a concentration 〉1.5 mmol/L was found to be more effective in reducing cellular viability than Fe（Ⅲ）, LDH release investigation suggests that Fe（Ⅱ） can reduce stability of the cell membrane. The activities of SOD and GPx of the cells treated with Fe（Ⅱ） were higher than those of the cells treated with Fe（Ⅲ）, although both of them increased with raising iron supply levels. The results indicate that both Fe（Ⅱ） and Fe（Ⅲ） could reduce the cellular antioxidase gene expression at high levels.