BACKGROUND:Various gene-delivery strategies have be used to transfer targeted genes into damaged bone tissues. As the most efficient gene vector, viral delivery systems have been used in bone tissue engineering research. OBJECTIVE: To thoroughly discuss the applications of different viral vectors in gene-enhanced bone tissue engineering. METHODS:A computer-based online search was performed in PubMed database for the related articles from January 2002 to January 2015. This review centered on viral vector transduction methods and their use in bone tissue engineering. Adenovirus, retrovirus, adeno-associated virus and chimeric virus were al discussed. Advantages and limitations of different vectors and their applicability toward bone tissue engineering were presented in this article. A total of 24 articles were included for review. RESULTS AND CONCLUSION:Current viral vectors for gene delivery in gene-enhanced bone tissue engineering are summarized, including recent work where combinatorial gene therapy is used to express groups of genes to stimulate bone regeneration. Future directions for this field are discussed, where viral vectors mediated gene expression systems wil be combined with cels such as mesenchymal stem cels seeded in synthetic scaffolds to repair bone loss. Gene-enhanced bone tissue engineering has more advantages than traditional tissue engineering; viral vectors contribute to higher gene transfection efficiency than normal vectors. Long-term clinical observation is needed for the safety of viral vectors used in gene-enhanced tissue engineering in the body. Viruses are stil the most efficient means by which exogenous genes can be introduced into seeds cels.

20 minutes), side branch occlusion, coronary dissection among the 3 groups. There were no differences in the complex or multivessels lesions either. Conclusion Significant elevation of CK and CK-MB after PCI may be associated with multivessels intervention, coronary dissection, side branch occlusion and micro-thrombus formation.

Objective To investigate the effects of constant magnetic field (CMF) on proliferation, apopto-sis and nitric oxide (NO) secretion of rat bone marrow-derived endothelial progenitor cells (EPCs) intervened by C-reactive protein (CRP). Methods EPCs were isolated from rat bone marrow by density gradient centrifugation and cultured on fibronectin-coated dishes. The cells were divided into five groups, i. e., control group, CRP (12 μg/ml) group, CRP plus CMF (0.1, 0. 5, 1.0 mT) groups. Samples were collected 24 hours after incubation. Cell proliferation was measured by MTT chromatometry. Apoptosis rate was detected by flow-cytometry. NO content of culture medium was measured by nitrate reductase method. Results As compared with control group, cell prolifer-ation in CRP group reduced significantly (0. 265±0. 008 vs 0. 316±0. 011, P < 0.05), NO secretion also de-creased significantly [(22.7±4.5) μmol/L vs (37.6±3.8) μmol/L, P < 0.05], cell apoptosis rate elevated sig-nificantly [(10.8±0. 8) % vs (4.2±0.5)% ,P < 0.05]. Cell proliferation in CRP plus 0. 5 mT or 1.0 mT CMF group (0. 295±0. 009,0. 302±0. 010) were much more than those in CRP group (P<0.05), NO secretion contents [(28.3±4.9) μmol/L, (29.2±5.6) μmol/L]were also much more than those in CRP group (P < 0.05) , apopto-sis rate [(7.4±0.5)% ,(6.9±0.6)%]was significantly lower than that in CRP group (P <0.05). Conclusion CMF at intensity of 0.5 mT and 1.0 mT can antagonize the effects of CR, promote proliferation of EPCs and secretion of NO and inhibit apoptosis rate of EPCs.

OBJECTIVE:To determine the dissolution of ibuprofen and paracetamol in soft capsules.METHODS:Phos?phate buffer(pH=7.2)was taken as a solvent with the rotating speed set at75/min,and sample taken time was45minutes.The dissolution degree of ibuprofen and paracetamol in soft capsules were determined by a RP-HPLC method.The chro?matographic column was CN column;the mobile phase was phosphate buffer(pH=6.6)-methanol(60∶40)with a flow rate of1.0ml/min,the detection wavelength at223nm and the column temperature at30℃.RESULTS:The linear calibration curves were obtained with a range of0.17～100.14?g/ml for paracetamol(r=0.9999,n=9)and0.21～124.86?g/ml for ibuprofen(r=0.9999,n=9)respectively;the average recoveries of the two compounds were99.62%(RSD=0.36%)and99.79%(RSD=0.49%)respectively.CONCLUSION:The determination method is simple,rapid,accurate and reliable,which can be applied to measure the dissolution content of ibuprofen and paracetamol in soft capsules satisfactorily.

PURPOSE: Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) are an inhibitor of receptor tyrosine kinases (RTKs) that was discovered in recent years, and many studies showed that LRIG1 is a tumor suppressor gene and may be related to tumor drug resistance. In this study, we explored whether LRIG1 protein expression can improve the chemosensitivity of glioma cells and what was its mechanism. MATERIALS AND METHODS: We collected 93 cases of glioma tissues and detected the expression of LRIG1 and BCL-2. We constructed a multidrug resistance cell line U251/multidrug resistance (MDR) and examined the change of LRIG1 and BCL-2 at mRNA and protein expression levels. LRIG1 expression was upregulated in U251/MDR cells and we detected the change of multidrug resistance. Meanwhile, we changed the expression of LRIG1 and BCL-2 and explored the relationship between LRIG1 and BCL-2. Finally, we also explored the relationship between LRIG1 and RTKs. RESULTS: LRIG1 was negatively correlated with BCL-2 expression in glioma tissue and U251/MDR cells, and upregulation of LRIG1 can enhance chemosensitivity and inhibit BCL-2 expression. Furthermore, LRIG1 was negatively correlated with RTKs in U251/MDR cells. CONCLUSION: These results demonstrated that LRIG1 can improve chemosensitivity by modulating BCL-2 expression and RTK signaling in glioma cells.
Astrocytoma/drug therapy/genetics/metabolism ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics/*physiology ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Glioma/drug therapy/*metabolism ; Humans ; Membrane Glycoproteins/metabolism/*physiology ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; RNA, Messenger/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism

PURPOSE: Cancer stem cells have recently been thought to be closely related to tumor development and reoccurrence. It may be a promising way to cure malignant glioma by using glioma stem cell-targeted dendritic cells as a tumor vaccine. In this study, we explored whether pulsing dendritic cells with antigens of glioma stem cells was a potent way to induce specific cytotoxic T lymphocytes and anti-tumor immunity. MATERIALS AND METHODS: Cancer stem cells were cultured from glioma cell line U251. Lysate of glioma stem cells was obtained by the repeated freezing and thawing method. Dendritic cells (DCs) were induced and cultured from the murine bone marrow cells, the biological characteristics were detected by electron microscope and flow cytometry. The DC vaccine was obtained by mixing DCs with lysate of glioma stem cells. The DC vaccine was charactirizated through the mixed lymphocyte responses and cell killing experiment in vitro. Level of interferon-gamma (IFN-gamma) in the supernatant was checked by ELISA. RESULTS: After stimulation of lysate of glioma stem cell, expression of surface molecules of DC was up-regulated, including CD80, CD86, CD11C and MHC-II. DCs pulsed with lysate of glioma stem cells were more effective than the control group in stimulating original glioma cells-specific cytotoxic T lymphocytes responses, killing glioma cells and boosting the secretion of IFN-gamma in vitro. CONCLUSION: The results demonstrated DCs loaded with antigens derived from glioma stem cells can effectively stimulate naive T cells to form specific cytotoxic T cells, kill glioma cells cultured in vitro.
Animals ; Antigens, Neoplasm/immunology ; Apoptosis ; Brain Neoplasms/*therapy ; Cancer Vaccines/*therapeutic use ; Cell Line, Tumor ; Cell Proliferation ; Dendritic Cells/*cytology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Glioma/*therapy ; Humans ; Interferon-gamma/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplastic Stem Cells/*cytology ; T-Lymphocytes, Cytotoxic/immunology

The hypoxia-inducible factor is a significant regulator of adaptive transcriptional response in hypoxia or hypoxia. Hypoxia-inducible factor (hypoXIA-inducible factor) loses its activity after hydroxylation by proline hydroxylase in a normoxic environment. Proline hydroxylase inhibitor is a kind of new small molecule oral preparation by inhibiting the proline hydroxylase, reducing the degradation of HIF, activating the hypoxia-induced way, adjusting including stimulates erythropoiesis, iron absorption and mobilization, angiogenesis, lipid, and glucose metabolism, inflammation, energy metabolism, cell growth and differentiation, and other physiological reaction, Showed more clinical benefits. In recent years, the application of proline hydroxylase inhibitors in the field of renal anemia has achieved apparent efficacy, and the research in the field of ischemic heart disease has also made significant progress in the future in the treatment of ischemic heart disease and other aspects of good application prospects.

OBJECTIVEIn order to enhance the yield of artemisinin, makes out the Artemisia annua adaptive area regional assignment in Guangxi. To ensure the nicety in study, on the base of literature study and experience on the spot, the article inspect the division result.

METHODBy document analysis and colleted data of A. annua, make out sample collect proceed and inspect the result of artemisinin content rank distribution in Guangxi.

RESULT AND CONCLUSIONResult of A. annua regional assignment is checked out in the article, the result passes the check by AQL (32, 4). The conclusions insure subsequence study and the A. annua sample collect. The result of artemisinin content rank distribution in Guangxi can be used in artemisinin production.

Antimalarials ; analysis ; pharmacology ; Artemisia annua ; chemistry ; Artemisinins ; analysis ; pharmacology ; China ; Plant Extracts ; analysis ; pharmacology

Objective:To estimate the incidence and mortality rates of prostate cancer in China in 2015.Methods:The data from 501 cancer registries in China collected by the National Cancer Center were reviewed and evaluated, and the qualified data were included in the final analysis. According to the national population data in 2015, the nationwide incidence and mortality of the prostate cancer were estimated. Chinese standard population in 2000 and world Segi′s population were used to calculate the age-standardized (ASR) incidence and mortality rates (ASR China and world, respectively).Results:After data review, the data reported by 368 registries were included in the final analysis, covering a total population of 309 553 499, accounting for 22.52% of the national population at the end of 2015. There were 72 thousand new prostate cancer cases estimated in China in 2015, with a crude incidence rate of 10.23/100 000. The ASR China and ASR world are 6.59/100 000 and 6.47/100 000, respectively, which is the sixth incidence of male malignant tumor.The estimated number of prostate cancer death was 3.07 thousand in China in 2015, with a crude mortality rate of 4.36/100 000; The ASR China and ASR world mortality rates were 2.61/100 000 and 2.65/100 000, respectively, which is the tenth leading cause of death in male malignant tumor.The ASR China incidence and mortality of prostate cancer in males were higher in urban areas (8.40/100 000 and 3.11/100 000) than those in rural areas (4.16/100 000 and 1.90/100 000). The incidence and mortality rates in the eastern areas (8.54/100 000 and 2.99/100 000) were higher than those in the central (5.28/100 000 and 2.34/100 000) and western areas (5.32/100 000 and 2.37/100 000) of China.Conclusions:The incidence and mortality rates of prostate cancer in China are lower than the global average, but there is an increasing trend. The incidence and mortality of prostate cancer in China have obvious regional differences.