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To investigate the correlation of single nucleotide polymorphisms (SNP) in arachidonate 5-lipoxygenase gene (ALOX5) rs2029253, rs2228064 and rs2228065 sites, 5-lipoxygenase activating protein gene (ALOX5AP) rs10507391, rs4769874 sites with the risk for genesis of adult myeloid leukemia.By the approval from the hospital ethics committee and the informed consent of participants. 150 patients with myeloid leukemia (ML) as ML group and 134 healthy people as the control group were selected. The genomic DNA was extracted from the samples. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) combined with directly sequencing, PCR-amplified products were applied to test the polymorphism of 5 sites in ALOX5 and ALOX5AP gene.A allele frequencies of ALOX5 gene rs2029253 site in the ML group and the control group were 43.0% and 34.3%, respectively. And the G allele frequencies in the ML group and the control group were 57.0% and 65.7%, respectively. The genotype distributions of AA, AG and GG in ALOX5 gene rs2029253 site in the ML group were 32.2%, 21.5% and 46.3% respectively. That in the control group were 15.7%, 37.3% and 47.0% respectively. The genotype AA and A allele frequency of ALOX5 gene rs2029253 site were linked with the increased risk of myeloid leukemia (OR=2.26, 95% CI: 1.43-4.56, P＜0.05; OR=1.44, 95% CI: 1.02-2.03, P＜0.05). And the genotype AG and allele G reduced the susceptibility to myeloid leukemia (OR=0.46, 95% CI: 0.27-0.78, P＜0.01; OR=0.69, 95% CI: 0.50-0.98, P＜0.05), however, the polymorphisms of ALOX5 gene rs2228064 and rs2228065 site not correlated with the risk of myeloid leukemia (P＞0.05). The A allele frequency of ALOX5AP gene rs10507391 site in the ML group and the control group were 30.7% and 36.2% respectirely. The genotype distribution rates of AA, AT and TT in ALOX5AP gene rs10507391 site in the ML group was 1.3%, 58.7% and 40.0% respectively, that in the control group were 9.7%, 53.0% and 37.3% respectively. The genotype AA of ALOX5AP gene rs10507391 site correlated with the decreased risk of myeloid leukemia (OR=0.13, 95% CI: 0.03-0.57, P＜0.05), but the polymorphism of ALOX5AP gene rs4769874 site not correlated with the risk of myeloid leukemia (P＞0.05).The genotype AA, AG and allele A, G of ALOX5 rs2029253, as well as ALOX5AP rs10507391 may be correlate with the susceptibility to myeloid leukemia.ALOX5、ALOX5AP基因多态性与髓系白血病易感性的关系.探讨花生四烯5-脂氧合酶基因（arachidonate 5-lipoxygenase gene，ALOX5） rs2029253, rs2228064和rs2228065位点以及5-脂氧合酶激活蛋白基因（5-lipoxygenase activating protein gene，ALOX5AP）rs10507391和rs4769874位点的单核苷酸多态性（single nucleotide polymorphisms，SNP）与髓系白血病发病风险的相关性.经医院伦理委员会批准、患者知情同意，选取150例髓系白血病患者为髓系白血病（ML）组，134例健康人群为对照组。提取基因组DNA，采用聚合酶链反应及限制性片段长度多态技术（PCR-RFLP）联合PCR 产物直接测序法检测ALOX5、ALOX5AP基因5个位点的基因型.ALOX5 基因rs2029253位点在ML组和对照组中的A等位基因频率分别为43.0%和34.3%，而等位基因G的频率分别为57.0%、65.7%；基因型AA、AG和GG在ML组中的分布频率分别为32.2%，21.5%和46.3%，而在对照组中的分布频率分别为15.7%, 37.3%和47.0%。基因型AA和等位基因A可能增加髓系白血病的发病风险（OR=2.26，95% CI：1.43-4.56，P＜0.05；OR=1.44，95% CI：1.02-2.03，P＜0.05）；基因型AG与等位基因G可能降低对髓系白血病的易感性（OR=0.46，95% CI：0.27-0.78，P＜0.01；OR=0.69，95% CI：0.50-0.98，P＜0.05）。而ALOX5基因rs2228064、rs2228065位点多态性在ML组与对照组间的分布差异无统计学意义（P＞0.05）。ALOX5AP基因rs10507391位点等位基因A在髓系白血病组和对照组中频率分布分别为30.7%和36.2%；基因型AA、AT和TT在ML组中分布频率分别为1.3%，58.7%和40.0%，在对照组中的分布频率分别为9.7%, 53.0%和37.3%；基因型AA可能降低髓系白血病的发病风险（OR=0.13，95% CI：0.03-0.57，P＜0.05）；而ALOX5AP rs4769874位点基因型与等位基因分布频率在ML组与对照组间的分布差异无统计学意义（P＞0.05）.ALOX5 rs2029253位点基因型AA、AG和等位基因A、G以及ALOX5AP rs4769874位点AA基因型与髓系白血病发病的遗传易感性相关.

Macrophages within tissues display a strong plastic ability in respond to environmental cues in both physiologic influences and disease. However, the macrophage phenotype and its distribution in the bone marrow biopsies (BMB) samples of human acute leukemia (AL) remain poorly understood. In this study, 97 BMB samples of patients with acute leukemia and 30 iron-deficiency anemias (IDA) as control group were evaluated with immunohistochemistry. In comparison with controls, the counts of CD68+, CD163+, and CD206+macrophages were remarkably increased in BMB samples of acute leukemia (P

Macrophages have emerged as a key player in tumor biology. However, their number and phenotype in human bone marrow of biopsy (BMB) samples of chronic myeloid leukemia (CML) and their association with disease progression from an initial chronic phase (CP) to accelerated phase (AP) to advanced blast phase (BP) are still unclear. BMB samples from 127 CML patients and 30 patients with iron-deficiency anemia (IDA) as control group were analyzed by immunohistochemistry. The expression levels of CD68, CD163, and CD206 in BMB samples of CML patients were significantly higher than those in the patients of control group (P<0.01), and we observed that their positive expression was gradually elevated during the transformation of CML-CP to AP to BP (P<0.01). However, the expressions of CD68, CD163, and CD206 in released group were downregulated and contrasted to these in control group; there exists statistical significance (P<0.01). The percentage ratio of CD163 and CD206 to CD68 was pronounced to be increasing from CML-CP to AP to BP (P<0.01). Hence, the higher proportion of CD68+, CD163+ and CD206+ macrophages in BMB samples can be considered a key factor for disease progression of CML patients. Targeting macrophages, especially the M2 phenotype may help in designing therapeutic strategies for CML.

Objective: To investigate the expression level of IARS2 gene in colon cancer tissues and various cell strains of the cancer; to explore cytologically the effect of IARS2 gene knockdown on proliferation, apoptosis and cell cycle of RKO cells in the cancer. Methods: Real-time, fluorescence-based quantitative PCR (qPCR) was used to detect the expression of IARS2 gene in human colon cancer and surrounding tissues and in various cell strains of the cancer; the RNA interference target of IARS2 gene was designed and the target was detected by Western blot; the IARS2-siRNA lentiviral vector was established and used to infect the RKO cells of colon cancer; qPCR was employed to determine the effect of gene knockdown; changes of the RKO cells in growth, apoptosis, cell cycle and clone formation were observed after IARS2 gene knockdown. Results: The expression of IARS2 gene was higher in human colon cancer tissues than in surrounding tissues; there was expression of IARS2 gene in colon cancer cells, and the expression level of IARS2 gene mRNA was higher in the RKO cells than in the SW480, HCT116, DLD1, HT-29 and SW620 cells. After infection of the RKO cells with IARS2-siRNA lentivirus, the expression of IARS2 gene was inhibited in the level of mRNA; proliferation rate of the RKO cells was significantly inhibited; the G1 phase arrest of the RKO cells was increased with less RKO cells in S phase; the apoptotic RKO cells increased significantly; and the number of colonies of the RKO cells reduced. Conclusion: The expression of IARS2 gene is different in human colon cancer and surrounding tissues; after knockdown of IARS2 gene, proliferation of the RKO cells is inhibited; there are more cells in G phase and fewer cells in S phase; apoptosis of cells is increased; and formation of colonies is reduced. IARS2 gene is probably a cancer-promoting gene.

To investigate the liver X receptors agonists T0901317's effect on expression of FAT/CD36 gene mRNA in adult human skeletal muscle cell.Myotubes from humans were exposed to different T0901317 concentrations (0, 0.5, and 1.0 micromol/L) for 24 hours before experiments were performed. Then the expression of FAT/CD36 mRNA in skeletal muscle cell of each experimental group was detected by SYBR Green I real-time quantitative polymerase chain reaction. The relative data were compared among groups by 2-delta delta Ct method.(1) The Ct mean of control group, T0901317 (0.5 micromol/L) group, T0901317 (1 micromol/L) group were analyzed and there was significant difference (P0.01). (2) The expression of FAT/CD36 mRNA with liver X receptors agonists T0901317 in human skeletal muscle cell in the T0901317 (0.5 micromol/L) group and T0901317 (1 micromol/L) group were 2.91 times and 3.03 times than the control group.The expression of FAT/CD36 mRNA in human skeletal muscle cell afer the treatment of liver X receptors agonists T0901317 is increased, so we may propose that T0901317 may increase the risk of resistance in adult human skeletal muscle.

to study the effect of human bone marrow derived mesenchymal stem cells (hMSCs) on cytokines secretion (IFN-γ, TNF-α, IL-10, IL-6, IL-4 and IL-2) of allogeneic DC-CIK cells (in co-culture of CIK cells with DC), which investigate the mechanism of immunoregulation induced by hMSCs.the hMSCs from bone marrow were isolated, expanded and identified by cell morphology, differentiation into neuron-like cells with NSE, fat-like cells with red-oil stain, and expression of CD29, CD44. The DC and CIK cells from peripheral blood were isolated, expanded and identified by CD1α, HLA-DR or CD3(+);CD56(+);. The hMSCs were co-cultured with DC-CIK cells according to ratio 1:10. The expression of the six cytokines in supernatant was evaluated by flow cytometry after 4 days of DC-activated CIK cells in co-culture with hMSCs.the hMSCs displayed a fibroblast-like morphology and the positive cells of CD29 and CD44 were 96.6%, 94.6%, which have the capacity of differentiation into neuron-like cells with expressed NSE as well as fat-like cells with red-oil stain positive. The expression of CD1α, HLA-DR in DC was (91.9 ± 10.04)% and (88.8 ± 8.92)%. The CD3(+);CD56(+); double positive cells in DC-CIK cells was (29.23 ± 12.23)% compared to CIK cells with (15.98 ± 2.49)%. The cytokines secretion of DC-CIK cells in co-culture with hMSCs was IFN-γ (135.05 ± 48.19) ng/L; TNF-α (11.33 ± 1.42) ng/L; IL-10 (10.15 ± 2.25) ng/L; IL-6 (494.63 ± 235.222) ng/L; IL-4 (7.07 ± 2.30) ng/L and IL-2 (1074.6 3 ± 303.74) ng/L. In control group (DC-CIK cells) the secretion of IFN-γ, TNF-α, IL-10, IL-6, IL-4 and IL-2 was (717.6 ± 248.15) ng/L; (17.78 ± 7.52) ng/L; (29.95 ± 12.76) ng/L; (8.03 ± 0.21) ng/L, (9.08 ± 3.07) ng/L as well as IL-2 1 250 ng/L.the secretion of IFN-γ and IL-10 were down-regulated. It probably implied that hMSCs had the effect of immunoregulation on DC-CIK cells.