Abstract Background Lipid and glucose metabolism abnormalities are associated with nonalcoholic fatty liver disease (NAFLD). The triglyceride–glucose (TyG) index is a recently developed indicator that can identify individuals at risk for NAFLD. However, the applicability of the TyG index for identifying NAFLD in patients with type 2 diabetes mellitus (T2DM) is unclear. The aim of this study was to investigate the ability of the TyG index to identify individuals at risk for NAFLD in the T2DM population. Methods A total of 2280 participants with T2DM were recruited in this cross-sectional study. The TyG index was calculated, and NAFLD was diagnosed by ultrasonography. Binary logistic regression models were used to evaluate the association of the TyG index, glycemic parameters and lipid parameters with NAFLD. Results Logistic regression analysis showed that the TyG index was significantly associated with NAFLD in subjects with T2DM, the odds ratio (OR) were 3.27 (95% confidence interval [CI], 2.03–5.27; P < 0.001) for NAFLD in the highest TyG quartile after adjustment for known confounders. In stratified analysis, an elevated TyG index were more remarkably associated with NAFLD in younger patients (< 65 years; OR, 2.35; 95% CI, 1.83–3.02; P < 0.001), females (OR, 2.69; 95% CI, 1.67–4.32; P < 0.001), patients with BMI < 25 kg/m2 (OR, 2.80; 95% CI, 2.01–3.91; P < 0.0001), and with lower high-density lipoprotein cholesterol (< 1 mmol/L; OR, 2.76; 95% CI, 1.98–3.83; P < 0.001). Conclusion The TyG index is significantly associated with NAFLD and shows superior ability for identify NAFLD risk compared with other lipid and glycemic parameters in T2DM.

When organic polymer-based drug nanocarriers become concentrated in macrophages, their influence on macrophage polarization has been rarely reported. This study prepared chitosan-based nanoparticles (CNs, 181.5 nm, +14.83 mV) and detected their impacts on macrophage reprogram. RT-PCR results showed in M1-like RAW264.7 cells (Mφ1), CNs decreased CD86 and iNOS expressions by 53.8% and 57.1%, and increased Arg-1 and IL-10 by 642.9% and 102.1%; in M2-like cells (Mφ2), CNs reduced Arg-1 and MR expressions by 70.7% and 93.0%, but increased CD86, iNOS and TNF-α by 290.4%, 86.2% and 728.6%; these results, consistent with cytokine secretions and surface CD86/CD206 expressions, showed CNs polarized Mφ1 and Mφ2 toward opposite type so as to improve the macrophage polarization homeostasis. In CCl4-induced mouse liver injury model, CNs reduced the hepatic Mφ1/Mφ2 ratio from 1.1 (model group) to 0.3, and then reduced the serum AST and ALT level by 42.3% and 39.0%; in mouse model of hepatocellular carcinoma, CNs decreased the number of CD163-positive cells and increased CD86-positive ones in tumor, and subsequently inhibited the tumor growth and metastasis. This study suggests CNs can improve the phenotype homeostasis of macrophages and subsequently promote the treatment of certain diseases such as liver injury and tumor.

In recent years, with increasing social pressure and irregular schedules, many people have developed unhealthy eating habits, which has resulted in an increasing number of patients with diabetes, a disease that cannot be cured under the current medical conditions, and can only be mitigated by early detection and prevention. A lot of human and material resources are required for the detection of the blood glucose of a large number of people in medical examination, while the integrated learning model based on machine learning can quickly predict the blood glucose level and assist doctors in treatment. Therefore, an improved LightGBM model based on the Bayesian hyper-parameter optimization algorithm is proposed for the prediction of blood glucose, namely HY_LightGBM, which optimizes parameters using a Bayesian hyper-parameter optimization algorithm based on LightGBM. The Bayesian hyper-parameter optimization algorithm is a model-based method for finding the minimum value of the function so as to obtain the optimal parameters of the LightGBM model. Experiments have demonstrated that the parameters obtained by the Bayesian hyper-parameter optimization algorithm are superior to those obtained by a genetic algorithm and random search. The improved LightGBM model based on the Bayesian hyper-parameter optimization algorithm achieves a mean square error of 0.5961 in blood glucose prediction, with a higher accuracy than the XGBoost model and CatBoost model.

Hippo通路由一系列激酶构成,在细胞增殖和凋亡过程中起重要作用.上皮细胞顶端-基底极性、平面细胞极性、机械张力和G蛋白偶联受体均可以调控该通路活性.越来越多的研究发现Hippo通路参与了动脉粥样硬化相关病理的发生发展,在这个过程中,内皮细胞、巨噬细胞和平滑肌细胞中的Hippo通路发挥着重要作用.本文主要针对Hippo通路的调控及其在As中的潜在作用作一综述,以期为As提供新的治疗靶点和途径.

目的 前期工作发现苦瓜蛋白(MD28)可上调THP-1源性泡沫细胞三磷酸腺苷结合盒转运体A1(ABCA1)的表达而减少胞内的脂质蓄积,但其机制不清楚.文章拟从转录后水平分析其作用机制.方法 首先用miRNA芯片技术分析经MD28干预后,50 mg/L ox-LDL处理48 h的THP-1源性泡沫细胞miRNA谱中下调1.5倍的microRNA (miRNA),并与Genecards调控ABCA1基因表达的miRNA比较,找到二者共同miRNA,然后以荧光素酶报告基因系统验证其靶基因关系.qRT-PCR检测ABCA1 mRNA和miR-23b-3p的表达水平,Western blot检测蛋白表达水平,油红O染色测定胞内脂质蓄积.结果 miR-23b-3p是miRNA芯片和Genecards的交集,靶基因验证实验证实ABCA1是miR-23b-3p的靶基因.MD28剂量(0 g/L、0.4 g/L、1.2 g/L、3.6 g/L、5 g/L)和时间(0h、6h、12h、24 h、48 h)依赖性地上调ABCA1 mRNA及蛋白的表达水平,以1.2 g/L作用12 h最为显著.ox-LDL上调miR-23b-3p表达且被MD28抑制,MD28能减少胞内脂质蓄积,miR-23b-3p的抑制剂可拮抗MD28对ABCA1表达和胞内脂质蓄积的作用.结论 MD28通过下调miR-23b-3p介导其促进THP-1源性泡沫细胞ABCA1表达、减少胞内脂质蓄积作用.

目的 研究发现母体表达基因3(MEG3)对HepG2细胞载脂蛋白(a)[Apo(a)]表达的调控作用及其机制.方法 用荧光素酶报告系统分析MEG3与miR-125a-5p的靶向性结合.采用实时定量PCR(qRT-PCR)检测高表达Apo(a)的HepG2细胞和低表达Apo(a)的SMMC7721细胞中MEG3的表达情况;向HepG2细胞转染MEG3,Western blot和qRT-PCR检测Apo(a)、TET2表达情况;采用小干扰RNA技术沉默TET2的表达.结果 ①MEG3与hsa-miR-125a-5p能互补性结合,荧光素酶报告基因系统分析结果证实了MEG3与hsa-miR-125a-5p结合的存在.②miR芯片结果表明,在HepG2细胞中,hsa-miR-125a-5p表达水平升高,是对照组的近1.5倍,MEG3在HepG2细胞和SMMC7721细胞中均有表达,但前者MEG3的表达水平显著低于后者.③MEG3抑制Apo(a)表达.④MEG3下调miR-125a-5p的表达,上调TET2的表达;miR-125a-5p的mimics可逆转MEG3对Apo(a)的下调作用及TET2的表达,但可被miR-125a-5p的抑制剂逆转;TET2沉默可逆转MEG3对Apo(a)的下调作用.结论 MEG3通过miR-125a-5p/TET2途径下调HepG2细胞Apo(a)的表达.

Objective Recent studies have revealed a link between toll-like receptors (TLRs), Kruppel-like factors (KLFs), and the adipose tissue inflammation associated with obesity. TLR4 is associated with chronic inflammation in obesity. KLF7 is known to play an important role in the differentiation of adipocytes, but its role in visceral adipose tissue inflammation has not yet been investigated. Thus, the objective of this study was to determine the correlation of TLR4 and KLF7 in inflammation induced by obesity. Methods A total of 32 Wistar male rat subjects were fed in the center for experimental animals of Shihezi University. The rats were divided into normal control (NC) and high-fat diet (HFD) group. Surgical instruments were used to collect rats’ visceral adipose tissue samples in the 10th week after HFD feeding. Ninety-five Uygur subjects between 20 and 90 years old were enrolled in the present study. The subjects were divided into two groups: the normal control group (NC, 18.0 kg/m2 ≤ BMI ≤ 23.9 kg/m2, n = 50) and the obesity group (OB, BMI ≥ 28 kg/m2, n = 45), and visceral adipose tissue was collected from the subjects. Anthropometric and clinical parameters were measured using standard procedures; biochemical indices were detected using the glucose oxidase-peroxidase method and a standardized automatic biochemistry analyzer; the plasma levels of inflammatory factors and adipocytokines were measured by enzyme-linked immunosorbent assay (ELISA); the mRNA and protein expression levels of key genes involved in the inflammatory signaling pathway were measured by real-time PCR and Western blot. Results In rats, compared with the NC group, the weight, Lee’s index, waist circumference, visceral fat mass, and the plasma level of Glu, TG, FFA, and TNF-α were higher in the HFD group, while the plasma levels of LPT and APN were significantly lower in the HFD group in the 10th week. Furthermore, compared with the NC group, visceral adipose tissue’s mRNA expression levels of TLR4, KLF7, and SRC were higher in the HFD group, and KLF7 was significantly positively correlated with LDL, TLR4, SRC, and IL-6 (P < 0.05). Meanwhile, in the Uygur population, the plasma levels of TG, LDL, and TNF-α in the OB group were significantly higher than those in the NC group (P < 0.05). Moreover, compared with the NC group, visceral adipose tissue’s mRNA expression levels of TLR4, KLF7, and SRC were significantly higher in the OB group (P < 0.05), and KLF7 was significantly positively correlated with TC, TLR4, MYD88, SRC, and IL-6 (P < 0.05); the protein expression levels of TLR4 and KLF7 were significantly higher than those in the NC group (P < 0.05). Conclusion Higher expression of TLR4 and KLF7 may play a vital role in the process of inflammation induced by obesity in visceral adipose tissue.

Repaglinide is an insulin secretagogue that often exhibits considerable interindividual variability in therapeutic efficacy. The current study was designed to investigate the impact of KCNQ1 genetic polymorphism on the efficacy of repaglinide and furthermore to identify the potential mechanism of action in patients with type 2 diabetes. A total of 305 patients and 200 healthy subjects were genotyped for the KCNQ1 rs2237892 polymorphism, and 82 patients with T2DM were randomized for the oral administration of repaglinide for 8 weeks. HepG2 cells were incubated with repaglinide in the absence or presence of a KCNQ1 inhibitor or the pcDNA3.1-hKCNQ1 plasmid, after which the levels of Akt, IRS-2 and PI(3)K were determined. Our data showed that repaglinide significantly decreased HOMA-IR in patients with T2DM. Furthermore, the level of HOMA-IR was significantly reduced in those patients with CT or TT genotypes than CC homozygotes. The KCNQ1 inhibitor enhanced repaglinide efficacy on insulin resistance, with IRS-2/PI(3)K/Akt signaling being up-regulated markedly. As in our clinical experiment, these data strongly suggest that KCNQ1 genetic polymorphism influences repaglinide response due to the pivotal role of KCNQ1 in regulating insulin resistance through the IRS-2/PI(3)K/Akt signaling pathway. This study was registered in the Chinese Clinical Trial Register on May 14, 2013. (No. ChiCTR-CCC13003536).

Objective To study the effect of milk enriched with phytosterol ester on blood cholesterol.Methods Participants with hypercholesterolemia were recruited from community health center and randomly assigned to 3 groups:milk enriched with phytosterol ester group (PS group,n =59),normal milk group (n =58) and non-dairy group (n =62).The intervention lasted for 2 months.At baseline,all subjects in the 3 groups received health education on prevention and control of hypercholesterolemia.For PS and normal milk groups,subjects consumed 500 g milk per day,the intake of phytosterol in PS group was 1.58 g/d.For non-dairy group,subjects did not consume any dairy products during the trial.Subjects were assessed on their physical activity level and blood cholesterols were measured during monthly follow-up.Results Finally 157 subjects completed the trial.By the end of the first month,the TC and LDL-C levels of PS group were significantly lower than that of normal milk group.After adjustment,there was no significant difference between baseline and 1-month TC levels in PS group.The levels of TG and HDL-C in PS group were significantly increased while the LDL-C level was significantly decreased after 1-month intervention.Compared with normal milk and non-dairy groups,no differences were observed for these four indicators.After 2-month intervention,the TC and LDL-C levels of PS group were significantly lower than that of normal milk and non-dairy groups.The levels of TC and LDL-C in PS group were significantly reduced compared to baseline levels after adjustment.TG level was increased while HDL-C level was unchanged.Compared with normal milk and non-dairy groups,the levels of TC and LDL-C in PS group were significantly declined while no significant difference was observed for TG and HDL-C levels.Conclusions Milk enriched with phytosterol ester has a notable effect on lowering TC and LDL-C levels in subjects with hypercholesterolemia.

Catechol-O-methyltransferase (COMT) plays a central role in DNA repair and estrogen-induced carcinogenesis. Many recent epidemiologic studies have investigated the association between the COMT Val158Met polymorphism and cancer risk, but the results are inconclusive. In this study, we performed a meta-analysis to investigate the association between cancer susceptibility and COMT Val158Met in different genetic models. Overall, no significant associations were found between COMT Val158Met polymorphism and cancer risk (homozygote model: odds ratio [OR] = 1.05, 95% confidence interval [CI] = [0.98, 1.13]; heterozygote model: OR = 1.01, 95% CI = [0.98, 1.04]; dominant model: OR = 1.02, 95% CI [0.97, 1.06], and recessive model: OR = 1.03, 95% CI [0.97, 1.09]). In the subgroup analysis of cancer type, COMT Val158Met was significantly associated with increased risks of bladder cancer in recessive model, and esophageal cancer in homozygote model, heterozygote model, and dominant model. Subgroup analyses based on ethnicities, COMT Val158Met was significantly associated with increased risk of cancer in homozygote and recessive model among Asians. In addition, homozygote, recessive, and dominant models were significantly associated with increased cancer risk in the subgroup of allele-specific polymerase chain reaction genotyping. Significant associations were not observed when data were stratified by the source of the controls. In summary, this meta-analysis suggested that COMT Val158Met polymorphism might not be a risk factor for overall cancer risk, but it might be involved in cancer development at least in some ethnic groups (Asian) or some specific cancer types (bladder and esophageal cell cancer). Further evaluations of more preclinical and epidemiological studies are required.

SummaryRepaglinide is a short‐acting insulin secretagogue, which often results in considerable interindividual variability in therapeutic efficacy when widely used in a clinical setting. Among various reasons under discussion is genetic polymorphism, especially the genes related to insulin secretion and resistance. Recent studies have described the importance of PPARD in regulating the secretion and resistance of insulin. However, little is known about the impacts of PPARD genetic polymorphism on the efficacy of repaglinide. Therefore, the current study was designed to investigate the associations of PPARD rs2016520 polymorphism with type 2 diabetes mellitus (T2DM) susceptibility and repaglinide therapeutic efficacy in Chinese Han T2DM patients. A total of 338 T2DM patients and 200 healthy subjects were genotyped for PPARD rs2016520 polymorphism by polymerase chain reaction–restriction fragment length polymorphism assay. A total of 84 patients with the same genotypes of CYP2C8*3 139Arg and OATP1B1 521TT were randomized to orally take repaglinide for 8 weeks. Then the pharmacodynamic parameters of repaglinide and biochemical indicators were determined before and after repaglinide treatment. No significant difference was found in either allelic frequency (P = 0.298) or genotype distribution (P = 0.151) of PPARD rs2016520 between T2DM patients and healthy subjects. However, T2DM patients carrying genotype TC showed a significantly lower increase in postprandial serum insulin (mU/L) than those with wild‐type TT (P < 0.05). These findings suggest that PPARD rs2016520 polymorphism might influence the therapeutic effect of repaglinide rather than T2DM susceptibility in Chinese Han T2DM patients.

神经生长因子是神经营养因子家族成员之一,对不同时期神经元的存活、分化、生长及损伤后的修复和再生都有着十分重要的作用.不仅在神经系统中,随着人类的其他正常和肿瘤组织中同样也检测得到了NGF,神经生长因子在各方面的应用也得到了重视并均已得到了证实.NGF功能的发挥离不开与其受体的结合,根据NGF表面糖蛋白与凝集素结合能力的不同,其受体可被分为高亲和力受体酪氨酸激酶A和低亲和力受体p75.TrkA与NGF结合后所介导的信号通路主要有:①MAPK通路;②PLC-γ通路;③PI3K/PKB通路.而p75与NGF结合介导的信号传导通路主要包括:①NF-κB通路;②JNK-p53-Bax凋亡通路;③神经酰胺通路.TrkA一般介导的是正性信号,如促进神经细胞生长、维持神经细胞的存活等;而p75既可促进神经细胞存活,也可诱导神经细胞凋亡,但以后者为主.当TrkA与p75同时表达时,TrkA可抑制p75诱导细胞凋亡,使受损神经细胞大量增殖,所以其生物学总效应是促进神经细胞的生长和存活.

Study ObjectiveTo investigate the associations of NOS1AP rs12742393 polymorphism with the risk of type 2 diabetes mellitus (T2DM) and repaglinide therapeutic efficacy in Chinese patients with T2DM.DesignProspective case‐control study.SettingAcademic medical center.PatientsA total of 300 patients with T2DM and 200 healthy volunteers were enrolled to identify NOS1AP rs12742393 genotypes using the polymerase chain reaction–restriction fragment length polymorphism assay. Eighty‐four patients with various genotypes were randomly selected to receive oral repaglinide as a single‐agent therapy (3 mg/day) for 8 weeks.Measurements and Main ResultsAnthropometric measurements and fasting plasma glucose (FPG), postprandial plasma glucose, hemoglobin A1c, fasting serum insulin (FINS), postprandial serum insulin, homeostasis model assessment for insulin resistance (HOMA‐IR), triglyceride, total cholesterol, low‐density lipoprotein‐cholesterol, and high‐density lipoprotein‐cholesterol tests were obtained before and after repaglinide treatment. The risk C allelic frequency of NOS1AP rs12742393 was higher in patients with T2DM than in healthy volunteers (p<0.001). Patients with T2DM and genotypes AA and AC at NOS1AP rs12742393 had a significant reduction in FPG (mmol/l) compared with those with genotype CC (p<0.01). Patients with CC homozygotes and AC heterozygotes had a greater increase in FINS (mU/l) than those with wild‐type AA (p<0.05). In addition, the carriers of genotype CC at NOS1AP rs12742393 had higher differential values of HOMA‐IR compared with genotypes AC and AA carriers (p<0.001). The effects of repaglinide treatment on FPG (p<0.01), FINS (p<0.05) and HOMA‐IR (p<0.001) were reduced in patients with T2DM carrying the NOS1AP rs12742393 risk C allele compared with the AA genotype carriers.ConclusionThe NOS1AP rs12742393 polymorphism is associated with therapeutic efficacy of repaglinide in Chinese T2DM patients.

Objective To investigate the correlation between PPAR-δ gene polymorphisms,type 2 diabetes mellitus and metabolic indicators in Chinese Han population of Huaihai area.Methods The subjects were divided into case group(200 patients with type 2 diabetes mellitus)and control group(200 healthy people).The PPAR-δ gene polymorphisms in all subjects were detected with polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)method.Heigh,weight,waist circumference(WC),hip circumference(HC),systolic blood pressure(SBP),diastolic blood pressure(DBP),fasting blood glucose(FPG),total cholesterol(TC),triglyceride(TG),high density lipoprotein cholesterol(HDL-C)and low density lipoprotein cholesterol(LDL-C)were measured,and the body mass index(BMI)and waist to hip ratio(WHR)were calculated in all subjects.Results There were no significant differences of the genotype frequency and allete frequency at PPAR-δ-87T/C site between two groups(P>0.05).There were significant differences of weight and BMI between different genotypes in patients with type 2 diabetes mellitus(P<0.05).The weight of cases with CC genotype was significantly higher than that of case with TT genotype,the BMI of cases with CC genotype was significantly higher than that of case with TT and TC genotypes(P<0.05 or P<0.01).There were no significant differences of other indexes among cases with 3 different genotypes(P>0.05).Conclusion There may be not the obvious correlation between the polymorphisms of PPAR-δ-87T/C and type 2 diabetes mellitus for Han redidents in Huaihai area,but PPAR-δ-87T/C gene polymorphisms may be associated with the obesity of patients with type 2 diabetes mellitus.

【Objective】To explore the effect of RhoA/ROCK signaling pathway to promote the growth of retinal ganglion cells(RGCs) axon by erythropoietin(EPO).【Methods】The models of optic nerve crush were established in the right eyes of 48 Sprague-Dawley rats after 3 days of Dil superior colliculus retrograde labeling of RGCs. The model rats were randomly divided into 3 groups and 16 rats for each, namely control group, EPO group and EPO+Y- 27632 group. After 15 days, survival number and density of RGCs were observed under fluorescence microscope by sections of retina; at the same time, the expression level of growth associated protein-43(GAP-43) was measured by Western blot, the expression level of RhoA and ROCK mRNA was detected by RT-PCR.【Results】Compared to the control group, the expression level of ROCK mRNA was decreased(P <0.01), but the expression level of GAP-43was significantly increased(P <0.01) in EPO group. Compared to EPO group, the expression level of ROCK mRNA was decreased(P <0.01), while the expression levels of GAP-43 and MAP-1B significantly were increased(P <0.01) by given the inhibitor Y-27632 of ROCK. 【Conclusion】The promotion to the growth of retinal ganglion cells(RGCs) axons by EPO was related to the activity downregulation of RhoA/ROCK signaling pathway.

Objective To investigate the correlation between KCNQ1 gene polymorphism and type 2 diabetes mellitus(T2DM) in Chinese Han population in Huaihai region.Methods 200 T2DM inpatients and outpatients admitted to the Department of Endocrinology of the Affiliated Hospital of Xuzhou Medical College were selected as case group and 200 healthy people underwent physical examinations in the same region and period were selected as control group.Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) method was used to detect gene polymorphisms in the two groups.Results(1) In the control group,the genotypes of CC,CT and TT in KCNQ1 rs2237892 accounted for 36.0%(72/200),51.0%(102/200) and 13.0%(26/200) respectively and the allele frequencies of C and T were 61.5%(246/400) and 38.5%(154/400) respectively.In the case group,the genotype frequencies of CC,CT and TT were 47.5%(95/200),44.0%(88/200) and 8.5%(17/200) respectively and the allele frequencies of C and T were 69.5%(278/400) and 30.5%(122/400).The genotype distribution and allele frequencies in KCNQ1 rs2237892 between the two groups showed statistically significant differences(P0.05).(2) The genotype distributions and allele frequencies in KCNQ1 rs151290 between the two groups showed no statistically significant differences(P0.05).Conclusion KCNQ1 rs2237892 polymorphism may be associated with the incidence of type 2 diabetes mellitus among Chinese Han population in Huaihai region.The polymorphism of KCNQ1 rs151290 may have nothing to do with the incidence of type 2 diabetes mellitus in Chinese Han population in Huaihai region.

Objective:To investigate the expressions of miR-23a and runt-related transcription factor 1(RUNX1) in gastric cancer and their significances. Methods:The binding affinity between the miR-23a and 3' untranslated region(3'UTR) of RUNX1 was evaluated by luciferase reporter gene activity assay.The resection specimens(gastric cancer tissues and their adjacent tissues) from 87 gastric cancer patients were collected,and then the expressions of miR-23a and RUNX1 were detected by in situ hybridization and immunohistochemical staining,respectively. Results:The uciferase reporter gene activity assay suggested that RUNX1 was the target gene of miR-23a.The positive expression rates of miR-23a and RUNX1 in the 87 cases of gastric cancer tissues were 82.76% and 14.94% respectively,and both were significantly higher than those(25.29% and 80.46%) in the adjacent tissues(both P0.01).The expression of miR-23a in the cases with lymph node metastasis was significantly higher than that in the cases without lymph node involvement(P0.01),and the miR-23a expression increased with the development of the clinical stage and infiltration depth(P0.01).The expression of RUNX1 in the cases with lymph node metastasis was significantly lower than that those without lymph node involvement(P0.01),and the RUNX1 expression decreased with the development of the clinical stage and infiltration depth(P0.01).There was a significant negative correlation between the expression of miR-23a and RUNX1 in gastric cancer(r=–0.474,P=0.004). Conclusion:RUNX1 is the target gene directly regulated by miR-23a.The high miR-23a expression and lower RUNX1 protein expression may be important biological markers for malignant transformation of the gastric mucosa,and invasion or metastasis of gastric cancer.

Since 1992 the theory of ecological footprint model has been concerned by more and more researchers.In recent twenty years,a great progress has been made in the study of ecological footprint all over the world,especially in China.In this paper we briefly introduced the concept and the calculation methods of ecological footprint,stated its weakness and advantage,and reviewed its research progress abroad and at home.Finally,we argued the possible future research directions of ecological footprint.

目的 探讨C-erbB-2在乳腺浸润性导管癌中的表达及临床意义.方法 采用免疫组化SP法检测63例乳腺浸润性导管癌中C-erbB-2的表达.结果 C-erbB-2在>50岁与≤50岁年龄组表达率分别为72.0%和60.5%,差异无统计学意义(P>0.05);在浸润性导管癌Ⅰ、Ⅱ、Ⅲ级中表达率分别为36.4%,66.7%,84.6%,在Ⅰ、Ⅱ级中明显低于Ⅲ级,差异有统计学意义(P<0.05);C-erbB-2在肿瘤直径>2 cm组与≤2 cm组表达率分别为59.5%和76.2%,差异无统计学意义(P>0.05);在淋巴结无转移组、转移组中表达率分别为69.4%,59.3%,差异无统计学意义(P>0.05).结论 C-erbB-2的表达与乳腺癌的组织学分级密切相关,与年龄、肿块直径及腋窝淋巴结转移无明显相关性.C-erbB-2的检测可作为乳腺癌预后判断的重要参考指标.

This study was aimed to investigate the effect of down-regulating the CXCR4 expression on cell cycle and cell apoptosis of human T-ALL Jurkat cells. The CXCR4 specific siRNA plasmid vector was constructed and then transfected into the cultured Jurkat cell line by DMRIE-C. The expression of CXCR4 mRNA was detected by RT-PCR, the cell distribution in cell cycle and cell apoptosis were determined by flow cytometry. The experiments were divided into 3 groups: group A (blank control), group B (non-silencing dsRNA as negative control) and group C (CXCR4 siRNA). The results showed that the expression level of CXCR4 mRNA in Jurkat cells transfected with CXCR4 siRNA (group C) decreased and cell proportion in G(0)/G(1) phase increased as compared with group A (56.9% +/- 1.4% vs 68.3% +/- 2.4% and 35.8% +/- 1.9% vs 18.1% +/- 1.2% respectively) (p < 0.01), cell proportion in G(2)/M and S phase decreased as compared with group A (19.8% +/- 1.7%, 44.4% +/- 2.1% vs 27.2% +/- 1.5%, 54.7% +/- 2.8% respectively) (p < 0.01). The apoptosis rate of Jurkat cells in group C increased as compared with group A (20.9% +/- 2.0% vs 3.13% +/- 0.9% respectively) (p < 0.01), and the comparison between group A and B showed no statistical difference. It is concluded that the CXCR4 specific siRNA can effectively down-regulate the CXCR4 mRNA expression, which induces the cell apoptosis and cell cycle arrest, thereby inhibits the Jurkat cell proliferation.