Rapid tumor cell growth depends on intracellular polyamine levels higher than those of normal cells. Intracellular polyamine depletion inhibits tumor cell proliferation and induces tumor cell apoptosis. Therefore, polyamine metabolism has recently been identified as an important target for anti-tumor therapy. This article briefly summarizes recent polyamine metabolism targeting, polyamine depletion within the tumor cells through a variety of methods, and the antitumor effects of the treatment.

As a major adhesion molecule of endothelial junction, vascular endothelial cadherin (VE-cadherin) plays a very important role for the maintenance of vascular homeostasis. It regulates infiltration of vascular endothelia on contents in plasma such as eukocytes and lipid, as well as cellular proliferation and apoptosis. It plays an important role by involving in angiogenesis in the multiple links of the process of atherosclerosis, This article reviews the recent progress in research on the effects and mechanisms of VE-cadherin in the occurrence and developmaent of atherosclerosis in recent years.

Objective To investigate whether difluromethylornithine (DFMO) can be used in the treatment of human leukemia. Methods The cell proliferation was detected by MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium)] assay after treatment of human lymphocyte Jurkat cells by DFMO (0 to 10 mmol/L) for 24 to 72 h. Enzyme activity of spermine oxidase (SMO) and acetylpolyamine oxidase (PAO) was determined by chemiluminesence assay. DNA fragmentation assay was used to evaluate cell apoptosis. Fluorescent dye assay was performed to determine the changes in mitochondrial membrane potential. Western blotting was used to determine Bax content. Casepase-3 enzyme activity was measured by spectrophotometric method. Results DFMO treatment inhibited the proliferation of Jurkat cells significantly in a dosage- and time-dependent manner (P

Aim To study the effects of polyamine analogue CPENSpm on the human lung cancer line A549 in cell proliferation and apoptosis.Methods MTS was used to assay the cell proliferation,chemical analysis methods were used to determine the activities of enzymes in the polyamine metabolism,HPLC was performed to assay the intracellular concentration of polyamines,Sub-G1 and DNA fragmentation assays were used to determine the cell apoptosis.Results Treating A549 lung cancer cells by CPENSpm resulted in:①cell-growth inhibition and cell apoptosis;②inhibition of ODC(key enzyme in polyamine synthetic pathway)and activation of SSAT and SMO(key enzymes in polyamine catabolism);③great decrease of intracellular polyamine concentrations.MDL72527,the SMO inhibitor,can antagonize the effect of CPENSpm on inhibiting the proliferation of A549 cells.Conclusion CPENSpm inhibits proliferation and induces apoptosis of human A549 lung cancer cell line by interfering the polyamine metabolism,depleting intracellular polyamine contents that are need by quick-growth of cancer cells and inducing production of H2O2.

Atherosclerosis is the major cause of ischemic stroke.Given the importance of the early diagnosis and intervention of atherosclerotic plaques,the use of molecular imaging techniques for early diagnosis of atherosclerosis has become a research focus in recent years.This article reviews the advances in research on molecular imaging in the aspect of early diagnosis of atherosclerosis.

Objective To investigate the effect of the new polyamine analogue tetrabutyl propanediamine (TBP) on cell proliferation and the underlying mechanism. Methods MTT assay was performed to determine cell proliferation. Flow cytometry was performed to detect cell cycle transition. DNA fragmentation and mitochondrial membrane potential determinations were performed to detect cell apoptosis. The activity of key enzymes in polyamine catabolism was detected by chemiluminescence assay. Results TBP could significantly inhibit the proliferation of HL-60 cells by blockingcell cycle transition and by inducing apoptosis. The TBP-induced apoptosis of HL-60 cells was in a dose-dependent manner. The enzyme activities of SMO and APAO were also significantly increased in HL-60 cells after treatment with 100 μM TBP for 24 hours. Conclusions TBP, as a new putrescine analogue, could inhibit proliferation of HL-60 cells by increasing the enzyme activity of SMO and APAO and inducing apoptosis.

Transient ischemic attack(TIA)is known as a risk warning signal of cerebral infarction. In order to screen the patients with high risk of TIA rapidly and give them correct and timely treatment, and thus prevent stroke, this article reviews the etiology, pathogenesis, clinical manifestation and imaging that affect on TIA, and the more commonly used prognostic rating scales at present.

AIM: To prepare recombinant human spermine oxidase (SMO) and polyclonal antibody against human SMO by gene recombination techniques. METHODS: Human SMO cDNA was amplified from total RNA of A549 cells through reverse transcription PCR. The cDNA was then cloned into pET-15b to construct SMO prokaryotic expression vector. After transforming, the vector was induced to express recombinant SMO by IPTG in E. coli BL21 (DE_3). Recombinant SMO was purified by Ni-NTA resin under denaturing condition and then was dialyzed to renature. The enzyme activity of recombinant SMO was analyzed by chemical fluorescent method. SMO polyclonal antibody was prepared by using recombinant human SMO protein purified by polyacrylamide gel electrophoresis as antigen to inoculate rabbit intradermally. The titer and specificity of anti-sera were determined by ELISA, Western blot and Immune Cell Chemistry. RESULTS: Purified and dialyzed recombinant human SMO has the specificicity of oxidizing the spermine. The polyclonal antibody has high titer and specificity against human SMO. CONCLUSION: This research established a method for prokaryotic expression, purification and polyclonal antibody preparation of human SMO. The method lays a foundation for the future functional research of SMO.

Objective To explore the repair result of full-thickness cartilage defects in diannan small-ear pig by bone mesenchymal stem cells (BMSCs) transferred with both transforming growth factor-β3(TGF-β3) and bone morphogenetic protein-2(BMP-2) gene mediated by adenovirus vector and combined with deminerized bone matrix (DBM). Methods 32 full-thickness defects from 16 knees of 8 pigs were randomly divided into 4 groups in the experiments. In group A, the animals′ lateral femoral condyle of right knee joint was repaired with DBM and BMSC infected with both Ad-TGF-β3 and Ad-BMP-2. In group B, the medial femoral condyle of right knee joint was repaired with DBM and BMSC without infection. In group C, the lateral femoral condyle of left knee joint was repaired with DBM. And the group D is control group. Morphology and histology were observed 2, 4, 8 and 12 weeks after operation. Results 12 weeks after operation, the whole defects were repaired in group A, HE staining showed typical cartilaginous structure in the repaired area. In group D, defects were not repaired but filled with fibrous tissue. The O′driscoll scores were 15.65 ± 0.11 (group A), 11.33 ± 0.22 (group B), 6.13 ± 0.15 (group C) and 5.08 ± 0.15 (group D). There was significant difference among the groups (P < 0.05). Conclusions The new type of tissue engineering scaffold that DBM combined with BMSCs transfected with both Ad-BMP-2 and Ad-TGF-β3 could induce cartilage regeneration and repair the defects.

Objective To explore the influence of peritumoral edema (PTE) on the tendency of recurrent location and morphological character after total resection using MRI. Methods MRI data was collected from 43 patients with recur-rent brain glioma after total resection from four clinical centers and then the influence of of PTE on recurrence patterns af-ter total resection was retrospectively analyzed based on the T2 weighted image. Results The PTE had a significant influ-ence on the recurrent patterns of brain gliomas after total resection. When PTE was mild, the shapes of recurrent gliomas tended to be focal (6/8) and the recurrent locations tended to be local (5/8). When PTE was severe, the shapes of the recur- rent gliomas tended to be spread(30/35 and the recurrent locations tended to be distant (25/35), followed by marginal (7/35), In addition, the morphological patterns and locations of recurrent gliomas were significantly different among different PTE types (all P<0.001). When PTE was ring shape, the shapes of recurrent gliomas tended to be focal (7/9) and the recur-rent locations tended to be local (6/9), followed by marginal (2/9) and distant (1/9). When PTE was irregular shape, most of recurrent locations tended to be distant (25/34), followed by marginal (7/34) but rarely local (2/34). Conclusions The de-grees and the types of brain glioma PTE can significantly influence the locations and morphological patterns of recurrent gliomas after total resection.