This is a review of recent progress in the study on environment sensitive hydrogel based on cyclodextrin and their most recent and relevant applications in the intelligent drug delivery systems. Based on relevant literatures, the development of environment sensitive hydrogel responsive to physical, chemical and biochemical stimuli was introduced, involving their categorization, design principles, mechanism of action and potential application. Various new types of intelligent drug delivery system, which responds to various triggers, could be constructed by using the cyclodextrin-based environment sensitive hydrogel. They made it possible to control the drug release freely. Although these hydrogels are still at their research stage, they have attracted considerable interest in the intelligent drug delivery system.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by non-cardiogenic,acute,progressive and hypoxic respiratory insufficiency or respiratory failure mediated by various internal and external stimuli.The pathogeny of lung injury is varied,pathogenesis is complicated,and it is not clear.Related pathogeny and pathogensis of lung injury is reviewed as follows.

Adenoviridae ; genetics ; Genes, p53 ; Genetic Therapy ; methods ; Genetic Vectors ; Humans ; Neoplasms ; therapy ; RNA Interference ; Tumor Suppressor Protein p53 ; genetics

OBJECTIVE:To observe the safety and immunological effects of Measles-mumps-rubella(MMR)attenuated live at-tenuated vaccine in children. METHODS:300 children aged 8-12 months receiving inoculation were selected from Changsha Hospi-tal for Maternal and Child Health Care during Jan. 2015-Apr. 2016 to observe safety and immunological effects. Those children were divided into MMR group,measles vaccine group,mumps vaccine group and rubella vaccine group according to vaccine type, with 75 cases in each group. The occurrence of ADR in 72 h were compared among 4 groups after inoculation;venous blood of chil-dren was collected before vaccination and 5 months after vaccination,and the antibody positive test was carried out by micro coagu-lation inhibition (HI) test;HI antibody titer was recorded after immunization,and positive rate and genometric meantiter(GMT) were calculated. RESULTS:The incidence of ADR in 4 groups were 9.33%,8.00%,8.00% and 10.67%,respectively. No local ADR was found in 4 groups;among systemic ADR,the incidence of fever was higher than that of other clinical manifestations,be-ing 4.00%,4.00%,4.00% and 5.33%;there was no statistical significance in the incidence of ADR among 4 groups(P>0.05). Measles,mumps and rubella antibody positive rates of MMR group were 100%,92.00% and 100%,respectively;antibody posi-tive rates of measles vaccine group,mumps vaccine group and rubella vaccine group were 100%,85.33% and 100%,respective-ly;there was no statistical significance in same antibody positive rate among 4 groups(P>0.05). GMT of measles in MMR group and measles vaccine group were 1∶41 and 1∶27,that of mumps in MMR group and mumps vaccine group were 1∶6.3 and 1∶6.2, there was no statistical significance (P>0.05);GMT of rubella in MMR group and rubella vaccine group were 1∶320 and 1∶849, with statistical significance (P<0.05). CONCLUSIONS:Compared to traditional single vaccine,MMR dose not increase the inci-dence of ADR and not influence positive rate,but GMT of rubella increases significantly,to which should be paid attention.

Anticancer drugs resistance is often ascribed to gene mutation,amplification or epigenetic changes that affect the uptake,metabolism or export of drugs at the cell level.Tumor physical microenvironment not only influences the drug distribution but also causes difference in cell proliferation rate and hypoxia or acidosis due to its heterogeneity,which could affect the tumor drug resistance.This review discusses the relationship between cancer physical microenvironment and drug resistance and the strategies for enhancement of the chemotherapy sensitivity through modification of the tumor physical microenvironments,as well as foreground of the research.

Neovascular glaucoma ( NVG ) is a kind of intractable eye disease with complex etiology, strong destruction and poor effect on treatment. Extensive retinal ischemia and hypoxia is the main etiology, and the key of treatment is early diagnosis, active prevention and taking effective measures to prevent the production of vascular endothelial growth factor. According to the related literature over recent years, the authors will discuss pros and cons for medical, surgical and combined treatment in this review.

Objective: To investigate the change in function of autophagy in hepatocarcinoma cell line HepG2 induced by Oxa (oxaliplatin), and to explore the role of autophagy in Oxa-induced cell death. Methods: The HepG2 cells were routinely cultured in vitro and treated either with different concentrations of Oxa alone or in combination with the autophagy inhibitor 3-MA (3-methyladenine ) or CQ (chloroquine). The cell viability was detected by CCK-8 (cell counting kit-8) assay. The formation of autophagosomes was observed directly under TEM (transmission electron microscope). Western-blotting was used to track the conversion of autophagic marker proteins LC3-I to LC3-II. Results: CCK-8 assay demonstrated that Oxa could dose-dependently induce the death of HepG2 cells, and when it was administrated in combination with 3-MA or CQ, Oxa could also significantly inhibit the growth of HepG2 cells. The formation of autophagosomes in HepG2 cells after Oxa treatment could be observed under TEM, as well as an increase in expression of LC3-II was found. The expression of LC3-II increased markedly after the inhibition of degradation pathway induced by CQ, which reflected an enhancement of autophagic flux induced by Oxa. 3-MA could inhibit the formation of autophagosomes in HepG2 cells. Conclusion: Oxa can enhance the function of autophagy in HepG2 cells and induce an increase in autophagosome formation. The autophagy inhibitors 3-MA and CQ can both facilitate the proliferative inhibition of hepatocarcinoma cell line HepG2 induced by Oxa, and they can also increase the antitumor effect of Oxa. Copyright © 2013 by TUMOR.

OBJECTIVE:To study the inhibitory effects of minocycline (MC) on TNF-α induced monocyte-endothelial adhe-sion and the relative mechanism. METHODS:Primary human umbilical vein endothelial cells (HUVECs) were isolated from hu-man umbilical veins with enzyme digestion. HUVECs were divided into blank control group,model group,MC low-dose,medi-um-dose and high-dose groups(1,10,100 μmol/L). After treated for 2 h,10 ng/ml TNF-α was employed to stimulate monocytes THP-1 adhesion with HUVECs except for blank control group,in order to induce monocyte-endothelial adhesion model. The num-ber of adherent cell was observed by fluorescence microscope,and fluorescence intensity was detected by microplate reader. Flow cytometry was adopted to detect the expression of intercellular adhesion molecule (ICAM)-1. The expressions of NF-κB p65 pro-tein in cell nucleus and cytoplasm were detected by Western blot. RESULTS:Compared with blank control group,the number and fluorescence intensity of adherent cell,the expression of ICAM-1 and the protein expression of NF-κB p65 in nucleus were all in-creased in model group,while the protein expression of NF-κB p65 in cytoplasm was weakened,with statistical significance(P<0.01). Compared with model group,the number and fluorescence intensity of adherent cell,the expression of ICAM-1 were all de-creased in MC low-dose,medium-dose and high-dose groups;the protein expression of NF-κB p65 in nucleus was weakened in MC medium-dose and high-dose groups,while the protein expression of NF-κB p65 in cytoplasm was heightened,with statistical significance (P<0.01 or P<0.05). CONCLUSIONS:MC can inhibit TNF-α induced monocyte-endothelial adhesion by a likely mechanism of reducing the expression of ICAM-1 in HUVECs and inhibiting the expression of NF-κB p65 protein.

Objective To observe the latency and amplitude characteristics of event-related potential P300 under different target stimu-lus. Methods During January to December, 2014, 35 patients with memory impairment received P300 test under the percentage of target stimuli of 0.10 and 0.25. The latency, amplitude and area under amplitude were compared. Results There was no significant difference in la-tency (t<0.256, P>0.800), but the amplitude and area under amplitude increased under 0.10 compared with those under 0.25 (t>4.259, P<0.05). Conclusion Less target stimulation may improve the patients' attention and increase amplitude of P300, but no more interference in la-tency, suggesting latency of P300 is more stable for assessment of cognitive function.

Objective: To study the influence of glycogen synthase kinase 3β (GSK3β) overexpression on the function of murine macrophage RAW264.7. Methods: Eucaryotic vector pcDNA3. 1-GSK3β was constructed and transfected into RAW264.7 cells via lipofectamine 2000. RAW264.7 cells stably expressing GSK3β were screened by G418 selection. Phagocytosis ability of RAW264.7 cells was assessed by neutral red analysis; the content of nitric oxide (NO) and the activity of tumor necrosis factor (TNF) in the supernatant of RAW264.7 cells stably expressing GSK3β were determined by Griess method and crystal violet staining assay, respectively. Results: RAW264.7 cells stably expressing GSK3β showed an inhibited phagocytosis ability, with the inhibitory rate being 20.4% (P<0.05), and an inhibited production of NO by RAW264.7 cells stably expressing GSK3β in presence of 1 μg/ml LPS, with the inhibitory rate being 25.6% (P<0.01). The transfected RAW264.7 cells had an increased production of TNF by 28.8% (P<0.01). Conclusion: GSK3β can regulate macrophages in inflammatory and immune responses.