目的 探讨芪灵扶正清解方(QFQ)对Huh-7细胞能量代谢及糖酵解相关蛋白的影响.方法CCK8法检测0、62.5、125、250、500 μg/mL QFQ醇提物干预Huh-7细胞24、48和72 h后的细胞活力.将Huh-7细胞分为0、62.5、125、250、500 μg/mL组,分别予相应浓度的QFQ醇提物干预24 h,应用细胞能量代谢分析仪检测线粒体和糖酵解ATP产生速率、实时耗氧率、胞外酸化率、糖酵解速率和质子流出速率;Western blot检测Huh-7细胞缺氧诱导因子1α(HIF-1α)、己糖激酶(HK)、葡萄糖转运蛋白(Glut)1以及Glut3的蛋白表达量.结果① 与0 μg/mL组比较,125、250、500 μg/mL QFQ醇提物干预Huh-7细胞24、48和72 h后细胞活力明显降低(P＜0.01).② 与0 μg/mL组比较,62.5、125、250 μg/mL组Huh-7细胞线粒体和糖酵解ATP产生速率比值明显提高(P＜0.05),125、250 μg/mL组Huh-7细胞糖酵解速率明显降低(P＜0.05或P＜0.01);与0 μg/mL组比较,随着检测时间延长,62.5 μg/mL组Huh-7细胞实时耗氧率呈升高趋势(P＜0.05),250 μg/mL组Huh-7细胞胞外酸化率和质子流出速率呈降低趋势(P＜0.05).③ 与0 μg/mL组比较,62.5、125、250、500 μg/mL组Huh-7细胞的HIF-1α、HK、Glut1、Glut3蛋白表达量均明显降低(P＜0.01或P＜0.05).结论 QFQ通过调控细胞能量代谢和糖酵解相关蛋白HIF-1α、HK、Glut1和Glut3的表达,提高线粒体能力,抑制糖酵解能力,促进有氧呼吸,从而有效抑制Huh-7细胞的增殖.

目的 观察蒲葵子乙醇提取物(EELC)对肝癌细胞以及裸鼠皮下移植瘤的抑制作用,探讨EELC阻滞细胞周期的抗肝癌作用机制.方法 培养人肝癌HepG2细胞,采用MTT法和平板克隆形成实验检测不同浓度EELC(0、0.125、0.25、0.5 mg/mL)对HepG2细胞活力和细胞周期的影响.构建裸鼠HepG2皮下移植瘤模型,将裸鼠随机分为对照组和EELC组,分别给予生理盐水和EELC灌胃液[3 g/(kg·d)]灌胃给药,连续21 d后,剥取肿瘤组织,采用免疫组织化学方法分析肿瘤组织中PCNA、CDK1、CyclinB1和p21的蛋白表达.结果 细胞实验结果显示,与0 mg/mL组比较,0.125、0.25、0.5 mg/mL组HepG2细胞活力和克隆形成率均明显下降(P<0.05),呈剂量依赖;与0 mg/mL组比较,0.125、0.25、0.5 mg/mL组细胞周期进程明显抑制,阻滞于G2/M期.动物实验结果显示,与对照组比较,EELC组小鼠肝癌组织PCNA、CDK1和CyclinB1蛋白表达明显降低(P<0.05),p21表达明显提高(P<0.05).结论 EELC通过促进p21表达,抑制PCNA、CDK1和CyclinB1表达,使细胞周期阻滞于G2/M期,抑制肝癌细胞增殖,进而抑制肝癌生长.

目的 探讨弥漫大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)患者血浆中的红细胞沉降率(e-rythrocyte sedimentation rate,ESR)在DLBCL预后判断中的价值.方法 收集81例初治DLBCL患者的ESR水平、临床特征及预后,对它们的关系进行回顾性分析.将患者分为ESR高水平组和正常组.应用Pearson Chi-Square检验比较两组患者临床特征的差异;Log-rank检验比较ESR水平的高低与总生存期(overall survival,OS)及无进展生存期(progression free survival,PFS)的相关性;Cox单因素和多因素回归分析比较DLBCL患者临床病理特征与预后的相关性.结果 在DLBCL中,ESR高水平与结外侵犯＞1处、更高的美国东部肿瘤协作组(Eastern Cooperative Oncology Group,ECOG)评分(2～4分)、更高的国际预后指数(International Prognostic Index,IPI)(3～5分)和国家综合癌症网络国际预后指数(National Comprehensive Cancer Network IPI,NCCN-IPI)(≥4分)有关.ESR高水平组较正常组OS和PFS均更短.Cox单因素回归分析提示:LDH水平升高、高ESR水平、更高的IPI评分和NCCN-IPI评分(4～5分),既是影响DLBCL患者OS的危险因素,也是影响PFS的危险因素,而更高的ECOG评分(2～4分)和结外侵犯＞1处是影响DLBCL患者OS的危险因素.多因素回归分析显示:LDH水平异常、结外侵犯＞1处是影响DLBCL患者OS的独立危险因素,GCB亚型是影响OS的独立保护因素;高ESR水平虽然不是影响OS的独立危险因素,却是影响DLBCL患者PFS的独立危险因素.结论 ESR高水平与DLBCL患者的不良预后相关,是DLBCL患者PFS的独立不良预后因素.

目的 从IL-6/STAT3信号通路角度探讨熊果酸(UA)调控人结直肠癌HT-29细胞增殖和凋亡的机制.方法 体外培养HT-29细胞,分空白组(不给药)、模型组(给予10 ng/mL的IL-6)和20、40、80μmol/L UA组(10 ng/mL的IL-6分别联合20、40、80μmol/L的UA).MTT法检测细胞活力;DAPI染色观察细胞凋亡形态;流式细胞术检测细胞凋亡率和细胞周期;比色法测定Caspase-3酶活力;平板克隆形成实验检测HT-29细胞的克隆形成能力;RT-PCR法检测Bcl-2、Bax、Cyclin D1、CDK4、p15的mRNA水平;Western blot法检测STAT3、p-STAT3、Bcl-2、Bax、Cyclin D1、CDK4和p15蛋白水平.结果 IL-6提高了HT-29细胞的生长活力和克隆形成能力,这一现象能被UA显著抑制;UA将HT-29细胞周期阻滞在G0/G1期,增加了HT-29细胞的凋亡率,激活了Caspase-3酶活力,抑制了因IL-6刺激而导致的Bcl-2、Cyclin D1、CDK4和p-STAT3蛋白水平的上调和Bax、p15基因或蛋白水平的下调.结论 UA可以通过抑制IL-6/STAT3信号通路调控其下游Bcl-2、Cyclin D1、CDK4、Bax、p15等因子的表达,进而有效抑制HT-29细胞的增殖、促进其凋亡.

目的 探讨松果菊苷(Echinacoside,ECH)对1-甲基-4-苯基吡啶离子(MPP+)诱导的人神经母细胞瘤细胞(SH-SY5Y)细胞氧化应激损伤的影响及机制.方法 选取对数生长期的SH-SY5Y细胞分为对照组(正常培养,不给予任何试剂干预)、MPP.+组(500 μmol/LMPP+处理细胞24 h)、ECH组(1、3、10、30 μmol/L ECH预处理细胞24 h后加500 μmol/L MPP+处理细胞24 h).CCK8检测细胞存活率,倒置相差显微镜观察细胞形态,Hoechst33342荧光染色法观察凋亡细胞,化学比色法检测抗氧化酶SOD、CAT活力以及脂质过氧化物丙二醛MDA含量.结果 与对照组相比,MPP+组细胞存活率显著下降;细胞生长状态明显变差;细胞内抗氧化酶SOD和CAT活力显著下降,MDA含量显著升高;出现明显细胞凋亡现象.松果菊苷预处理SH-SY5Y细胞24 h后,与MPP+组比较,细胞存活率显著上升;细胞生长状态明显好转;细胞内SOD、CAT活力显著上升,MDA含量明显减少;细胞凋亡现象明显缓解.结论 松果菊苷对MPP+诱导氧化应激损伤的SH-SY5Y细胞具有保护作用,可通过增强细胞内源性抗氧化酶的活力、抑制脂质过氧化物的生成来抑制细胞凋亡.

目的 探讨艾拉莫德对类风湿关节炎患者17型辅助性T细胞(Th17)与调节性T细胞(Treg)失衡的调节作用.方法 选取2016年6月至2017年1月住院的活动期类风湿关节炎患者74例,随机分为A组44例和B组30例.B组给予安慰剂口服,A组给予艾拉莫德口服,两组均坚持服药24周.采用流式细胞术检测外周血Th17和Treg细胞比例;采用酶联免疫吸附技术检测血浆Th17和Treg细胞分泌的相关细胞因子;治疗前后对患者进行DSA28,ACR20,ACR50和ACR70等综合疾病临床评分.结果 A组治疗24周后DSA28评分较治疗前有明显改善,差异有统计学意义(P<0.05);治疗24周后A组DSA28评分及ACR20,ACR50,ACR70改善情况均优于B组,差异有统计学意义(P<0.05).治疗24周后,A组外周血中Th17细胞(CD4+IL-17+)比例相较于治疗前降低,但差异无统计学意义(P>0.05),而Treg细胞(CD4+CD25+)比例相较于治疗前显著升高,差异有统计学意义(P<0.05);治疗24周后,B组外周血中Th17细胞比例无明显改变,Treg细胞比例略有升高,但与治疗前比较,差异无统计学意义(P>0.05).治疗24周后,A组促炎细胞因子IFN-γ、TNF-α、IL-17A水平较治疗前显著降低,差异有统计学意义(P<0.05);治疗24周后,B组促炎细胞因子IFN-γ、TNF-α、IL-17A水平较治疗前升高,差异有统计学意义(P<0.05).结论 艾拉莫德可通过下调Th17细胞,上调Treg细胞来恢复类风湿关节炎患者内环境细胞稳态,从而缓解疾病进展.

Fuzheng Qingjie (FZQJ) granules, a compound Chinese medicine, have been used as an adjuvant therapy for alimentary tract cancers. However, the underlying anticancer mechanisms are still not well understood. In the present study, HepG2 cells were treated with FZQJ-containing serum. Cell proliferation was evaluated using MTT assay. Apoptosis was analyzed using a flow cytometer. Cell ultrastructure was observed under a transmission electron microscope. The mitochondrial membrane potential (Δψ) was examined with JC-1 dye. In H22 tumor–bearing mice, CD4 + T cells, CD8 + T cells, CD3 + T cells, and natural killer (NK) cells in peripheral blood were evaluated cytometrically. Interleukin (IL)-2 and tumor necrosis factor (TNF)-α levels were measured using radioimmunoassay.The mRNA levels of Bax and Bcl-2 were examined by reverse transcription–polymerase chain reaction. The protein levels of Bax, Bcl-2, cytochrome C, caspase 3 and 9, PARP, and CD69 were examined by Western blotting. The apoptotic cells in tissues were observed using TUNEL method. Alanine transaminase (ALT), aspartate transaminase (AST), blood urea nitrogen (BUN), and creatinine (CRE) were detected by an automatic biochemical analyzer. The results showed that FZQJ-containing serum remarkably inhibited proliferation of HepG2 cells in dose- and time-dependent manners, induced HepG2 cell apoptosis and caused a decrease of Δψ. Analysis of tumor tissue showed that FZQJ-induced apoptosis was accompanied by downregulation of Bcl-2 and upregulation of Bax, release of cytochrome c, activation of caspase 3 and 9, and cleavage of PARP. In addition, FZQJ increased the percentages of CD4 + T and NK cells, the ratio of CD4 + /CD8 + T cells as well as the levels of serum TNF-α. FZQJ also increased CD69 expression in tumor tissue. No hepatorenal toxicity was observed in H22 tumor–bearing mice. These results indicated that FZQJ could inhibit the growth of hepatoma cells via regulating immune function and inducing mitochondria mediated apoptosis.

顺式AB（ cisAB）血型是ABO亚型中特殊的，而且相对常见的一种表现型，是ABO血型表观遗传学不符合孟德尔规律的AB亚型，可表现为O型父亲（母亲）和AB型的子女［1］。定型上可表现为ABO血型正反定型不符，从而导致ABO血型鉴定和配血困难，以及父权纠纷等问题。在胎母免疫方面也曾有cisAB血型引起ABO新生儿溶血病的报道［2］。对cisAB血型分子机制的研究有利于正确认识cisAB血型及其检测方法的改进，在安全输血、器官移植、产前胎儿ABO-HDN预测以及亲子鉴定等方面具有十分重要的作用。cisAB血型在NCBI中血型抗原基因突变数据库（ BGMUT ）中注册的等位基因有9种［3］，其分子机制尚未完全阐明。

Objective To evaluate the effect of hedyotis diffusa willd on phosphoinositide 3 kinase(PI3K),pro-tein kinase B(Akt)protein and phosphorylated Akt(p-Akt)protein expressions in nude mice with hepatic carci-noma transplanted subcutaneously. Methods Nude mice xenografts were established. The mice were randomly divid-ed into 2 groups:the hedyotis diffusa willd group and the vehicle group,which received hedyotis diffusa willd(6 g·kg -1 ·d -1 ,intragastric administration)and normal saline( intragastric administration),respectively. After 4 weeks of treatment,the tumors were harvested and weighed. The levels of PI3K,Akt and p-Akt proteins were ob-served with immunohistochemical staining. Results The tumor weight of the hedyotis diffusa willd group were high-er than that of the vehicle group(t = 4. 270,P = 0. 006). The gray levels of PI3K,Akt and p-Akt in the hedyotis dif-fusa willd group(118. 67 ± 8. 44,105. 19 ± 4. 718,96. 34 ± 5. 72)were also higher than those in the vehicle group (82. 00 ± 2. 72,72. 37 ± 2. 89,87. 99 ± 4. 16)(t = 0. 209,P = 0. 049;t = 2. 050,P < 0. 001;t = 4. 123,P =0. 002). The expressions of PI3K,Akt and p-Akt proteins were suppressed significantly by hedyotis diffusa willd. Conclusion Hedyotis diffusa willd could inhibit angiogenesis in hepatocellular carcinoma via regulating the PI3K/ Akt pathway.

Objective:To investigate the clinical effect of fixed point rotating neck method treating cervical spondylotic radiculopathy. Methods:100 patients with cervical spondylotic radiculopathy were randomly divided into treatment group and control group, treatment group was treated with fixed point rotating neck method, and control group with computer program-controlled tractor. Results:the total efficiency of treatment group was 100%, significantly higher than that of control group by 90%(P=0.000006<0.01);integral and SF-MPQ pain rating index scores of the two groups af-ter treatment were significantly higher than those before treatment, and treatment group significantly better than control group (P<0.01);both without adverse reactions. Conclusion:Fixed point rotating neck method treating cervical spondylotic radiculopathy is effective and without obvious adverse reaction, being worthy of promoting.

目的观察淫羊藿对认知障碍型大鼠雌二醇、睾酮、皮质醇的影响。方法3月龄Wistar大鼠48只，采用双侧颈总动脉永久结扎法（2-VO）制作认知障碍型大鼠，淫羊藿和阳性中成药银杏叶片给药15d。 ELISA检测大鼠外周血雌二醇、睾酮、皮质醇。结果在雄鼠，雌二醇水平4组之间无统计学意义（P＞0.05）；但睾酮水平4组之间有显著性差异，模型组睾酮水平显著高于空白组（P＜0.01），而淫羊藿显著降低睾酮水平（P＜0.01），与空白组比较无显著性差异（P＞0.05）。在雌鼠，模型组雌二醇水平显著高于空白组（P＜0.05），淫羊藿组雌二醇水平仍高于空白组（P＜0.05），4组睾酮、皮质醇水平无统计学意义（P＞0.05）。结论淫羊藿可降低雄性模型大鼠增高的睾酮水平，调节性激素水平，这为探讨认知障碍与神经内分泌关系，研发改善认知障碍的中成药提供了新思路。

目的：观察定点旋颈手法对神经根型颈椎病疼痛的改善效果。方法神经根型颈椎病患者100例，随机分为观察组和对照组各50例。观察组予定点旋颈手法治疗，对照组予电脑程控牵引器牵引治疗，隔天1次，10 d为1个疗程，共治疗2个疗程。治疗前后分别采用疼痛等级计分和视觉模拟评分（ VAS）评估疼痛情况。记录两组治疗期间不良反应发生情况。结果两组治疗后疼痛等级评分均低于治疗前，且观察组治疗后疼痛等级评分低于对照组、治疗前后评分差值高于对照组（ P均＜0．01）。两组治疗后VAS均低于治疗前，且观察组治疗后VAS低于对照组（ P均＜0．01）。两组治疗期间均未出现不良反应。结论定点旋颈法治疗神经根型颈椎病可明显减轻患者疼痛，效果较好。

Jiedu Xiaozheng Yin (JXY) is a Chinese herbal decoction used to treat hepatocellular carcinoma (HCC). Previous studies have demonstrated that JXY can inhibit HCC cell proliferation via induction of G0/G1 phase arrest. In this study, we investigated whether the inhibitory effect of JXY on HCC cells is associated with the inhibition of the Wnt/β‑catenin pathway and the polycomb gene product Bmi1. Ethyl acetate extract from JXY (EE-JXY) was prepared. Methyl thiazolyl tetrazolium (MTT) and colony formation assays were used to measure cell proliferation. Immunofluorescence was used to analyze the expression and location of β-catenin and Bmi1. Immunohistochemistry was used to examine the expression of proliferating cell nuclear antigen (PCNA), c-myc and cyclin D1. β-catenin, Bmi1, c-myc, cyclin D1 and p16INK4A mRNA levels were detected by RT-PCR. The results demonstrated that EE-JXY inhibited the expression of PCNA, c-myc, cyclin D1 and Bmi1, and upregulated the expression of p16INK4A. We also found that EE-JXY could facilitate β-catenin translocation from the cytoplasm and nuclei to the cytomembrane. Finally, suppression of cell proliferation and expression of Bmi1 and Wnt/β-catenin by EE-JXY was confirmed in a mouse xenograft model of HCC. Thus, EE-JXY can inhibit the proliferation of HCC partially via suppression of the Bmi1 and Wnt/β-catenin signaling pathways.

Fuzheng Qingjie (FZQJ) recipe is a polyherbal Chinese medicine capable of suppressing tumor growth and is used as an adjuvant therapy for various types of cancer. However, its anticancer mechanisms are yet to be fully elucidated. In the present study, we explored whether p38 mitogen-activated protein kinase (MAPK) was involved in FZQJ-mediated mitochondria-dependent apoptosis in human hepatocellular carcinoma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were used to measure the viability of HepG2 cells. 4,6-Diamidino-2-phenylindole (DAPI) and Annexin-V fluorescein isothiocyanate (FITC) were used to analyze the apoptosis of HepG2 cells. The mitochondrial membrane potential (∆ψ) and phosphorylated P38 MAPK protein were examined by a flow cytometer following 5,5',6,6'-tetrachloro‑1,1',3,3'-tetraethylbenzimidazolcarbocyanine iodide (JC-1) and Alexa Fluor® 647 mouse anti-phosphorylated P38 MAPK antibody staining, respectively. The activation of caspase-9 and caspase-3 were measured using colorimetric assays. Additionally, Bcl-2 and Bax expression were examined using reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis. The results demonstrated that water extract of FZQJ was able to induce apoptosis of HepG2 cells in vitro. FZQJ-induced apoptosis was accompanied by the loss of ∆ψ, downregulation of Bcl-2 and upregulation of Bax expression, and the activation of caspase-3, -9 and P38 MAPK. These results indicated that FZQJ induced apoptosis in HepG2 cells at least via P38 MAPK activation and the mitochondria-dependent apoptotic pathway.

目的 探讨白花蛇舌草抗人肝癌细胞株HepG2增殖的作用机制. 方法 体外培养人肝癌细胞株HepG2,MTT法检测HepG2细胞的增殖活力,流式细胞术检测HepG2细胞周期,相对荧光定量PCR检测细胞周期蛋白依赖性激酶2 (cyclin-dependent kinase,Cdk2)和核转录因子E2F1 mRNA的表达. 结果 HepG2细胞的存活率随着给药浓度的增大而降低,抑制作用呈现剂量依赖性;和空白组比较,给药组G0/G1期细胞百分含量明显升高(P＜0.05),S期细胞百分含量明显减少(P＜0.01),PI指教明显减少(P＜005),Cdk2和E2F1 mRNA水平显著下调(P＜0.01或P＜0.05). 结论 白花蛇舌草可能通过下调Cdk2和E2F1的mRNA表达,将HepG2细胞阻滞在G0/G1期,从而抑制HepG2细胞的增殖.

Hedyotis Diffusa Willd (HDW), a Chinese herbal medicine, has been widely used as an adjuvant therapy against various cancers, including hepatocellular carcinoma (HCC). However, the underlying anticancer mechanisms are yet to be elucidated. In the present study, the anticancer effects of HDW were evaluated and the efficacy and safety of HDW combined with low-dose 5-fluorouracil (5-FU) were investigated. HepG2 cells were cultured in vitro and nude mouse xenografts were established in vivo. The proliferation of HepG2 cells was measured using the MTT method and flow cytometry. The mRNA and protein expression levels of cyclin-dependent kinase 2 (CDK2), cyclin E and E2F1 were examined using relative quantitative real-time PCR and western blot analysis, respectively. The results showed that water extract of HDW remarkably inhibited HepG2 cell proliferation in a dose-dependent manner via arrest of HepG2 cells at the G0/G1 phase and induction of S phase delay. This suppression was accompanied by a great decrease of E2F1 and CDK2 mRNA expression. In addition, HDW remarkably potentiated the anti-cancer effect of low-dose 5-FU in the absence of overt toxicity by downregulating the mRNA and protein levels of CDK2, cyclin E and E2F1. Our findings support the use of HDW as adjuvant therapy of chemotherapy and suggest that HDW may potentiate the efficiency of low-dose 5-FU in treating HCC.

Objective To investigate the effect of Hedyotis Diffusa Willd combined with low-dose 5-fluorouracil(5-FU) on VEGF and TGF-β expressions in mice with hepatic carcinoma transplanted subcutaneously.Methods Hepatic carcinoma xenografts were established in nude mice and the mice were randomly divided into three groups,i.e.vehicle group(saline),low-dose 5-FU group(10 mg/kg·d-1) and combination group(10 mg/kg·d-1 5-FU plus 6 mg/kg·d-1 Hedyotis Diffusa Willd).After 4 weeks of treatment,tumors were harvested and weighed.VEGF and TGF-β were examined by immunohistochemistry.Results The tumor inhibitory rates of low-dose 5-FU group and combination group were higher than that of vehicle group.And the expression of VEGF and TGF-β were suppressed significantly by both 5-FU alone and in combination of Hedyotis Diffusa Willd,especially the later.Conclusion Hedyotis Diffusa Willd could potentiate the inhibitory effect of low-dose 5-FU on VEGF and TGF-β expressions,which may account for their antiangiogenesis effect.

Objective To study the relationship of Th1/Th2 cytokines level and patients with gastrointestinal cancer including deficiency and excess symptom,and to search the objective index of the deficiency and excess symptoms.Methods The 100 patients with gastrointestinal cancer were used in this test.These patients were divided into two groups:58 cases of the excess symptom group and the 42 cases of deficiency symptom group.Another 40 healthy people were used as the contrasting group.Several experimental indexes of blood were examined using ELISA,such as interleukin(IL)-2,-4,-6,-10 and interferon(IFN)-γ.Results The imbalance of Th1/Th2 type cytokines and the higher levels of Th2 type cytokines were expressed in the deficiency and excess symptom groups.Compared with the excess symptom group,the imbalance was remarkably statistic differences in the deficiency symptom group(P<0.05 or <0.01).Conclusion Th1/Th2 type cytokines have close correlation with gastrointestinal cancer including deficiency and excess symptoms,and the level of Th1/Th2 can be used as objective index of the deficiency and excess symptoms in gastrointestinal cancer.

Objective To study the effect of C-reactive protein(CRP)and peripheral blood leucocyte in pediatric patients suffering from upper respiratory infection.Methods CRP and peripheral blood leucocyte was detected respectively in 102 cases of pediatric patients suffering from upper respiratory infection and 20 cases of normal children.Results The results showed that the contents of CRP and peripheral blood leucocyte in bacterial infection group were significantly higher than those in the normal group(P0.05),and showed no significant difference between viral the infection group and the normal group(P0.05).Among the 67 cases of pediatric patients suffering from upper respiratory infection,43 cases were CRP positive and 31 cases were peripheral blood leucocyte positive,and the difference was significant(P0.05).CRP level was correlated with the peripheral blood leucocyte(r=0.346,P0.01).Conclusion The detection of CRP and peripheral blood leucocyte can be used to distinguish bacterial infection from viral infection.They may coordinate with each other in the procession of infection and may be used to guide clinical proper drug usage.