Immunotherapy, particularly lung cancer vaccine therapy, has advantages of less side effects and low costs over classi-cal therapies of lung cancer, such as surgery, radiotherapy, and chemotherapy, as well as the relatively new molecular targeting therapy. PhaseⅢclinical trial for many kinds of non-small cell lung cancer (NSCLC) vaccines is ongoing based on deeper understanding of im-mune system and the expression of tumor antigens. This review summarizes the development of NSCLC vaccines.

MicroRNAs are endogenously expressed non-coding RNAs, which are composed of approximately 18 nucleotides to 25 nucleotides. Mature microRNAs regulate gene expression by base pairing with the 3'-untranslated region of target mRNAs. These mature microRNAs can degrade target mRNAs or inhibit translation. This process is a type of post-transcriptional regulation of gene ex-pression. Studies have shown that microRNAs are important in physiological and pathological processes, such as cell proliferation, cell differentiation, and cell death. This article provides an overview of the function of microRNAs in the regulation of macrophages.

Objective To study the effects of Irinotecan (CPT-11) on human colorectal cancer HCT-116 and HT-29 cells and investigate the potential mechanisms.Methods The effect of Irinotecan on the proliferation of HCT-116 and HT-29 cells was determined by MTT assays.The invasive capacity was measured by transwell assays,and the apoptosis of the tumor cells was detected by flow cytometry after stained with Annexin-V and PI.The difference between the current of ATP-sensitive potassium ion of HCT-116 and HT-29 was examined by patch clamp.Results It was found that 1.0-64.0 μg/ml CPT-11 could inhibit the proliferation and the invasive capacity of HCT-116 and HT-29 cells at both dose-and time-dependent manner.The IC_(50) of HCT-116 and HT-29 were 39.3 and 19.5 μg/ml respectively.Cytometry showed that the apoptotic rates were increased from 14.8% and 9.3% to 36.9% and 27.9% after the treatment of 32.0 μg/ml and 16.0 μg/ ml CPT-11,which were close to their IC_(50).The proportion of G_0/G_1 and S of HCT-116 and HT-29 was enhanced from 27.4% and 17.4% to 95.9% and 98.2%.Transwell assay indicated that the invasiveness of HCT-116 and HT-29 was reduced by 40.8% and 47.5%.The patch clamp showed that CPT-11 reduced the I_(KATP) of cell membrane at a negative dose-dependent manner.Conclusion CPT-11 could have a significant impact on the proliferation,invasiveness,cell cycle,and the apoptosis of human colorectal cancer cell HCT-116 and HT-29.HT-29 was more sensitive to CPT-11 than HCT-116.The inhibitory effect of CPT-11 on cell proliferation might be linked to its inhibition of ATPsensitive potassium channel.

Objective To discuss the effects and mechanisms of tetramethylpyrazine(TMP)on learning and memory abilities of Alzheimer's disease(AD)mice.Methods The animal models of AD were induced by aluminium trichloride(AlCl3)intragasticly for forty days.Then,TMP was intragastricly administered for twenty days.The escape latency of the mice in water maze test was recorded;and AChE and SOD activities and MDA levels in the brain were detected by chemical eoiorimetrie method.The expressions of At3 and NF-κB in the cerebral cortex were measured by immunohistochemistry method.Results 1)TMP has markedly decreased escape latency in AlCl3 induced AD mice(P＜0.05).2)In the brain of AlCl3 induced AD mice,TMP reduced AChE activity 19%[(1.37±0.13)U·mgpro-1vs(1.69±0.27)U·mgprot-1,P=0.016],decreased MDA levels 34% [(43.63 4-13.27)nmol·mgprot-1 vs(28.59±8.52)nmol·mgprot-1,P=0.023]and increased SODD activity 39%[(55.81±10.25)U·mgprot-1 vs(40.04±13.06)U·mgprot-1,P=0.026],respectively.These resuits showed significant difference with model mice group(P＜0.05).3)TMP also decreased AB and NF-κB expressions in the cerebral cortex of AD mice models(P＜0.05).Conclusion In AlCl3 induced AD mice,TMP can remarkably enhance the learning and memory abilities,presumably in relation to raise the activity of SOD,reduce the activity of AChE,the levels of MDA and the expressions of AB and NF-κB in the brain.

Objective To investigate the effects and potential mechanism of irinotecan (CPT-11), an antitumor drug, on human colorectal cancer cell line HT-29 and its impact on 4-amion pyridine (4-AP), a kalium ion channel blocker. Methods The effects of CPT-11, 4-AP and combination of two drugs on proliferation and invasion of HT-29 cells were measured by MTT and Transwell assay respectively. The impact of CPT-11 or 4-AP on cell apoptosis was determined by flow cytometry with Annexin-V and PI staining. The current of ATP sensitive potassium ion (IKATP) was measured by patch clamp. Results The CPT-11 could inhibit proliferation of HT-29 cells at dose from 1.0 to 64.0 μg/ml in dose-and time-dependent manners. Whereas the above effect was enhanced when CPT-11 combined with 4-AP (1.0 mmol/L). The administration of CPT-11 (16.0 μg/ml) or 4-AP (1.0 mmol/L) significantly induced the cell apoptosis and inhibited the invasion of HT-29 cells, furthermore, these effects could be enhanced by combination of two drugs. And the different concentrations of CPT-11 reduced the IKATP of cell membrane in negative dose-dependent manner. Conclusions The effects of CPT-11 on HT-29 cells, such as reducing proliferation and invasion as well as inducing the apoptosis, can be enhanced by 4-AP, which may be related to inhibition of ATP-sensitive potassium channels.

Hypoxia and hypoxia-induced factors (HIFs) are main regulators for tumor stem cells, metastasis-initiating cells and their differentiated progenies to adapt to the environment which lacks oxygen and nutrient in the process of cancer development. HIFs are up-regulated in many tumors, including leukemia, glioblastoma, melanoma, prostate cancer, breast cancer and pancreatic cancer, in where they are especially highly expressed in hypoxic regions. HIFs activation can induce expression of numerous stem cell related genes and multidrug resistance genes, which may play important roles in tumour and stem cell-mediated self-renewing, energy metabolism alternation, invasion, metastasis, angiogenesis and treatment resis?tance of neoplastic cells. Consequently, it will provide new clues for cancer therapy after investigating the role of HIFs in tar?geted regulation and metabolic pathway modulation in various stem cell-mediated tumor cells.

Objective Acute spinal injury(ASI) is a kind of disease commonly seen in the orthopedic department, with secondary pathological injury causing the delayed damage of tissue structure. This study is focused on finding the injury mechanism of endothelin and the relation with calcium in SCI, and developing an effective treatment of SCI through animal experiment for clinic application in the future. Methods ASI animal model with radioimmuolo gical techniques are applied to examine the level of endothelin, and to find the pathological changes under microscope and electron-microscope. Results The quantity of endothelin and calcium in the cell with 1, 4-dihydropyridine calci um channel inhibitor is decreased, as a result, depolarization was lightened. The mechanism delays the development of secondary injury significantly. Conclusion This type of treatment may be used in emergency for spinal cord injury in order to protect the function and to gain much precious opportunity for spinal recovery and other treatment.

Qian Hu is the roots of Peucedanum praeruptorum Dunn. The object of the present paper was to determine the effects of water extract (QH-I) and petroleum ether extract (QH-M) of Qian Hu on smooth muscle contractility of isolated rabbit pulmonary artery rings. QH-I and QH-M antagonized pulmonary artery rings conlraction elicited by NE as well as KCl.QH-I and QH-M caused relaxation of rabbit pulmonary artery rings precontracted with NE as well as KCl. The contraction dose-response curves of pulmonary artery rings with NE were shifted to the right and the maximal contraction response were inhibited 73.1 ?8.0% and 43 .6? 4.2% by 1 .6 ? 10-5% and 8.0 ? 10-5%, QH-M, pD'2 = 4.72 ?0.43. These results indicate that Qian Hu may relax pulmonary artery smooth muscle directly as a Ca2+ antagonist

Objective: To study the effect of docetaxet (DOC) combined with 4-AP on human breast can-cer MCF-7 cells and to explore whether 4-AP could strengthen the effect of docetaxel. Methods: MTT assays were performed to investigate the effect of docetaxel, 4-AP and the combination of them on the proliferation of MCF-7 cells. Flow cytometry was employed to detect cell cycles and cell apoptosis after the cells were stained by PI alone or by Annexin-V and PI. Results: Docetaxel could significantly inhibit the proliferation of MCF-7 cells in a dose- and time- dependent manner. 4-AP could inhibit the proliferation of MCF-7 cells and the inhibitory rates were 11.9%±1.7%, 42.1%±3.2%, and 44.2%±1.6% at 24h, 48h and 72h after adding 4-AP. Moreover 4-AP (5mmol/L) could strengthen the effect of docetaxel. 4-AP (25μmol/L) could increase the effect of Docetaxel. Docetaxel at 5μmol/L could significantly increase the percentage of cells at G_2/M (53.58%± 1.44% vs. 8.83%±0.44%, P<0.01) and decrease the percentage of cells at G_0/G_1 (11.48%±0.14% vs. 63.89%±0.98%, P<0.01), indicating that docetaxel blocked MCF-7 cells at G_2/M phase. 4-AP at 5mmol/L could in-crease the percentage of MCF-7 cells at G_0/G_1 and decrease the percentage of cells at G_2/M (0.42%±0.17% vs. 8.83%±0.44%, P<0.05). Docetaxel could significantly increase late apoptosis and death of MCF-7 cells af-ter treatment over 24h (from 6.97%±0.75% to 20.77%±0.75%, P<0.05). Docetaxel combined with 4-AP could increase early apoptosis rate from 4.60%±0.91% to 12.20%±0.82% (P<0.05) and could increase late apopto-sis rate and death rate from 4.60%±0.91% to 12.20%±0.82% (P<0.05). Conclusion: Both docetaxel and 4-AP can inhibit the proliferation of MCF-7 cells. Docetaxel can increase the percentage of cells at G_2/M phase and 4-AP can increase the percentage of cells at G_0/G_1 phase. 4-AP could strengthen the inhibitory effect of docetaxel on the proliferation of MCF-7 cells through inducing cell apoptosis.

Objective:To test the effects of propofol on intracellular calcium free concentration ([Ca~(2+)]i) and inositol 1,4,5-triphosphate (IP_3) biological synthesis induced by norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in aortic smooth muscle cells (ASMC)of rats for the mechanism of relaxtion of propofol on vascular smooth muscle.Method: Using the flurospectrophotometry and Fura-2/AM loading method,the changes of [Ca~(2+)]i levels in primary culture ASMC were measured,and using the specific, IP_3 assay system and isotope radioactive protein binding experiment IP_3 production levels in aortic smooth muscle were measured. Result:The baselines of [Ca~(2+)]i was decreased when primary culture ASMC was pretreated with propofol in 72 hours. Propofol inhibited [Ca~(2+)]i increase induced by NE and 5-HT in dose-dependent way. With extracellular calcium free or calcium channel blocker(Verapamil),inhibition of propofol on NE and 5-HT increasing [Ca~(2+)]i levels were decreased,but could not be cancelled. Propofol depressed IP_3 biological synthesis induced by NE and 5-HT in dose-dependent way. Conclusion:Relaxation of propofol on aortic smooth muscle is closely related to inhibiting IP_3- induced calcium release to decrease intracellular calcium concentration.