Objective To explore the apoptosis of K562/G01 cells induced by triptolide through MDM2/p53 signaling pathway. Methods K562/G01 cell line was treated with different concentrations of triptolide. MTT was used to detect the cell proliferation inhibition rate. FCM was used to determine the apoptosis rate changes in 12 h and 24 h. The mRNA expression levels of bcr-abl, XIAP, MDM2, p53 were detected by real-time quantitative PCR. Results After treatment by 10, 20, 40, 80, 100 nmol/L TP in 12, 24, 48 h, the viability of K562/G01 cells was inhibited in time-dose dependence manner. K562/G01 cells was treated by 20 nmol/L, 40 nmol/L TP after 12 h, 24 h, the cell apoptosis rate was rising with drug concentration and time. The bcr-abl, XIAP, MDM2 mRNA expression was down-regulated and p53 mRNA expression was up-regulated by TP. Conclusion TP can inhibit the growth of K562/G01 cell line and induce apoptosis through XIAP-MDM2-p53 signaling pathway.

Objective To study the effect of La on antioxidase activity and ROS content in crucian liver stressed by cadmium.Methods The crucian were randomly divided into the control group, the 0.5 mg/L Cd2+exposed group and the low(0.5 mg/L Cd2++0.25 mg/L La3+),moderate(0.5 mg/L Cd2++0.5 mg/L La3+),high(0.5 mg/L Cd2++1 mg/L La3+)La3+ intervention groups.The activity of SOD,CAT and ROS activity in crucian liver was detected on the first day, the third day and the fifth day.Results The CAT and SOD activity in the Cd2+exposed group was higher than that in the control(P

ObjectiveTo observe the effect of Qishen Tongluo Zengzhi decoction on cognitive impairment in patients with acute phase of ischemic stroke.Methods A prospective randomized controlled trial was conducted, and 130 patients with acute phase of ischemic stroke and cognitive impairment accompanied by Qi deficiency and blood stasis and stagnationof phlegm-dampness syndrome admitted into the Neurology and Rehabilitation Departments of Rizhao Hospital of Traditional Chinese Medicine(TCM) Affiliated to Shandong University of TCM were randomly divided into treatment group and control group, 65 cases in each group. In the two groups, conventional internal treatment was given to all patients, and in the treatment group, additionally the Qishen Tongluo Zengzhi decoction was administered orally(composition: astragalus membranaceus 30 g, radix pseudostellariae 30 g, notoginseng 10 g,spatholobus stem 25 g, hirudo 3 g, pberetima 10 g, radix paeoniae rubra 12 g, Chinese angelica 12 g, peach kernel 10 g, carthamus tinctorious 10 g, achyranthes 12 g, radix rhapontici 10 g, rhizoma alismatis 6 g, Acorus gramineus Soland 9 g, polygala root 9 g, rhizoma cyperi 10 g, herba siegesbeckiae 15 g),one dose a day. While in the control group, oxiracetam 4.0 g intravenous drip was given, once a day. The whole course was 21 days in both groups. Before and after treatment, the cognitive function of all the patients in two groups was assessed by Mini-Mental State Examination(MMSE)and Montreal Cognitive Assessment(MoCA) scores, and incubation period and amplitude of P300 wave were recorded.Results Finally 62 cases were in treatment group and 63 cases in control group. Before treatment, the comparisons of the MMSE score, MoCA score and P300 latent period and amplitude between the two groups had no statistically significant differences(allP>0.05). After treatment in the two groups, the MMSE score, MoCA score and P300 wave amplitude were elevated, P300 latency period was shortened compared with those before treatment, and the changes were more prominent in treatment group〔score of MMSE: 25.33±2.32 vs. 21.68±2.29, score of MoCA(score): 26.61±3.06 vs. 22.40±2.93, P300 wave incubation period(ms): 349.62±20.01 vs. 371.87±19.63, P300 wave amplitude(μV): 8.70±2.92 vs. 5.72±2.33,allP<0.01〕.ConclusionQishen Tongluo Zengzhi decoctioncan effectively intervene cognitive impairment in patients with acute phase of ischemic stroke, and improve their cognitive function.

The build-in low-pressure monolithic column combined with hydride generation atomic fluorescence spectrometry ( HG-AFS ) was employed for speciation analysis of fish meat. The sample pretreatment and separation approach could be accomplished within 30 min. The proper amount of fish sample was weighed and smashed into puree. The extraction solution composed of 10% HCl, 1% thiourea, and 0. 15% KCl was added before loaded into the automatic temperature controlled vertex system with 2000 r/min. The sample solution was separated through Merck monolithic column, with 3% ( V/V) acetonitrile, 30 mmol/L amonium acetate and 0. 03%(V/V) 2-mercaptoethanol (2-ME) as the eluent. The after-column eluent was digested by novel UV digestion device with pipeline sintered into the lamp, and then detected by hydrid-generation AFS. The rapid LC separation enabled fast mercury speciation of fish sample within 10 min. The different UV lamp digestion effects, eluent components, carrier gas, shield gas, lamp current, as well as PMT working power was optimized. Under the optimal conditions, the robust system achieved detection limits (DL) of 0. 15 μg/L and 0. 14 μg/L for methylmercury and HgⅡ, respectively. The RSD (n=7) was less than 5%, the linear correlation coefficient was 0 . 999 , and the matrix spiked recovery was in the range of 85%-110% for Hg speciation. This method was used for the determination of Hg speciation in fish and soil samples, and was proofed to be a reliable, easy approach for daily inspection.

Aim Our previous study has found that ur-solic acid( UA) increased intracellular reactive oxygen species ( ROS ) production and adenosine monophos-phate-activated protein kinase ( AMPK ) phosphoryla-tion, inhibited signal transducer and activator of tran-scription 3 ( STAT3 ) phosphorylation and cyclooxygen-ase-2 ( COX-2 ) expression in gastric cancer cells . However , the molecular mechanism by which UA in-hibits COX-2 expression in gastric cancer cells has not been fully clarified .In this study we aimed to further clarify the signal transduction pathways involved in the UA-mediated inhibition of COX-2 expression in gastric cancer cells .Methods Human gastric cancer cell lines SGC-7901 and MKN-45 were routinely cultured in RPMI-1640 medium supplemented with 10% heat-in-activated fetal calf serum .Sub-confluent cell cultures were pre-treated with antioxidant N-acetylcysteine ( NAC) , AMPK activator 5-amino-4-imida-zolecarbox-amide-riboside ( AICAR ) , AMPK inhibitor compound C, or STAT3 inhibitor WP1066 and then treated with or without UA for 24 h.The expression of AMPK and phosphorylated AMPK ( p-AMPK ) , STAT3 and phos-phorylated STAT3 ( p-STAT3 ) , as well as COX-2 was detected by Western blot analysis .Results Antioxi-dant NAC and AMPK inhibitor compound C blocked UA-induced inhibition of STAT 3 phosphorylation and down-regulation of COX-2 expression in gastric cancer cells.Both AMPK activator AICAR and UA inhibited STAT3 phosphorylation and COX-2 expression; the combination of two drugs resulted in further reduction . STAT3 inhibitor WP1066 did not affect UA-induced AMPK phosphorylation , whereas it inhibited STAT3 phosphorylation and COX-2 expression .The inhibitory effects on the STAT3 phosphorylation and COX-2 ex-pression were significantly enhanced when SGC-7901 and MKN-45 cells were treated simultaneously with WP1066 plus UA.Conclusion UA inhibits COX-2 expression in gastric cancer cells , which may be medi-ated through ROS/AMPK/STAT3 signal transduction pathway .

Objective To investigate the effects of asymmetric dimethylarginine (ADMA) on apoptosis and phosphorylation of c-jun N-terminal kinase (JNK) in endothelial outgrowth cells (EOCs). Methods The mononuclear cells were harvested from umbilical cord blood by ficoll density gradient centrifugation, and induced into EOCs and then expanded in vitro. The identified EOCs were treated with different concentrations of ADMA (0, 1, 5, 10, 20 μmol/L) for 48 h. The adherent cells were treated with 10 μmol/L ADMA,then different concentrations of JNK specific inhibitor SP600125 (0, 5,10,20 and 40 μmol/L) were added and incubated for 48 hours. Caspase-3 activity was measured by microplate reader. Apoptotic incidences of EOCs were quantitatively determined by flow cytometry. The expression of Caspase- 3 and phosphorylase-JNK (p-JNK) were detected by Western blot assay. Results The treatment of ADMA (1-20 μmol/L) significantly induced apoptosis in EOCs by enhancing Caspase-3 express and also induced phosphorylation of JNK (P<0.05). Meantime, the JNK specific inhibitor SP600125 could attenuate the apoptosis induced by ADMA during this process (F=6.733,P<0.05) and inhibit the expression of Caspase-3 and p-JNK. Conclusion ADMA can induce apoptosis in EOC, which may be achieved by activating JNK signal transduction pathway.

Objective: To investigate the clinicopathological characteristics and their relationship with the prognosis of gastric neuroendocrine carcinoma (G-NEC). Methods: Medical records of 46 patients with G-NEC between January 2009 and September 2015 were reviewed to investigate the clinicopathological characteristics and their relationship with prognosis of G-NEC. Results: Univariate analysis showed that the factors including age, Borrmann classification, TNM stage, M stage, Ki-67 index, surgical approach, liver metastases, serum carcino-embryonic antigen (CEA) level and postoperative chemotherapy were related with the prognosis of G-NEC (all P < 0.05). The multivariate analysis showed that the age, surgical approach, serum CEA level and postoperative chemotherapy were the independent prognostic factor of the prognosis (all P < 0.05). Conclusion: G-NEC is a rare tumor with high degree of malignancy and poor prognosis. Patients with high serum CEA level have poor prognosis, and postoperative chemotherapy and surgical outcomes also affect the prognosis of G-NEC.

Objective To investigate the differences of X-ray findings of skeletal fluorosis between coal-burning type endemic fluo-rosis and industrial fluorosis.Methods The patients were randomly selected as research objects including 60 cases of coal-burning type endemic osteofluorosis and 60 cases of industrial osteofluorosis.The X-ray findings on the left forearm,crus and pelvic radio-graphs of these patients were analyzed retrospectively to find out the differences between skeletal fluorosis of coal-burning type endemic fluorosis and industrial fluorosis.Results X-ray features are no significant statistical differences between coal-burning type endemic fluorosis and industrial fluorosis,except these of interosseous membrane ossification of forearm and crus (forearmχ2=10.909,P<0.05;crusχ2=8.547,P<0.05),obturator membrane ossification of pelvis (χ2=36.554,P<0.05),periosteal proliferation outside bone of crus (χ2=4.937,P<0.05),and ossification of soleus (χ2=4.904,P<0.05).Conclusion The X-ray signs of endemic osteofluorosis and industrial skeletal fluorosis are almost similar,but there are some differences between them.

Background: Previous study has found that ursolic acid (UA) inhibited the proliferation of gastric cancer cells by the down-regulation of cyclooxygenase-2 (COX-2) expression.However,its molecular mechanism is not fully clear.Aims: To investigate the role of adenosine monophosphate-activated protein kinase (AMPK)/signal transducer and activator of transcription 3 (STAT3)/COX-2 signaling pathway in UA-mediated inhibition of gastric cancer cells proliferation.Methods: AMPK-pLVX,AMPK-shRNA,STAT3-pLVX,STAT3-shRNA plasmids were constructed,and then were transfected into human gastric cancer cell lines SGC-7901 and MKN-45,respectively.Gastric cancer cells were cultured with different concentrations of UA for different times.The expressions of phosphorylated AMPK (p-AMPK),phosphorylated STAT3 (p-STAT3) and COX-2 were measured by Western blotting,and cell proliferation was detected by CCK-8 assay.Results: UA dose-and time-dependently increased p-AMPK expression,inhibited p-STAT3 and COX-2 expressions in SGC-7901 and MKN-45 cells.Knockdown of AMPK blocked UA-induced inhibition of STAT3 phosphorylation and COX-2 expression.Overexpression of STAT3 blocked UA-induced down-regulation of COX-2 expression.Knockdown of AMPK and overexpression of STAT3 blocked UA-induced inhibition of proliferation of gastric cancer cells.Conclusions: UA may inhibit the proliferation of gastric cancer cells via down-regulation of COX-2 expression through AMPK/STAT3 pathway.