This work summarizes the research development and molecular mechanism of Ebp1, a member of the proliferation-associated 2G4 family, in tumor proliferation and invasion. This research serves as a basis and support for further research on the mechanism of tumor proliferation and invasion. The low expression of Ebp1 in various cancers promotes tumor proliferation and invasion. Ebp1 inhibits E2F1, cyclin D1, and cyclin E transcription by interacting with Rb, human histone deacetylase 2, and the transcriptional repressor Sin3A. This inhibition triggers cell cycle arrest and suppresses cell proliferation. Ebp1 also influences cancer invasion and migration. However, the underlying mechanisms remain unknown and require further exploration.

Objective To explore any protective effect of hyperbaric oxygen in traumatic brain injury and its effect on the expression of silent information regulator 1 ( SIRT1) . Methods Sixty mice were randomly divided into a control group (n=20), a brain injury group (TBI, n=20) and a hyperbaric oxygen therapy group (TBI+HBO, n=20) . The mice in the TBI and TBI + HBO groups were given massive blows to establish closed brain injuries, while in the control group the scalp was incised and a bone window was removed without brain damage. The mice in the TBI + HBO group were given hyperbaric oxygen treatment twice per day for five days, while those in the TBI and control groups were put in the hyperbaric chamber but not given HBO treatment. At one hour after the trauma and on 5 days afterward, the neurological functioning of the mice was measured to generate neurological severity scores. Brain tissue was resected for triphenyl tetrazolium staining to measure the infarct area. Cortical neurons were isolated to eval-uate the SIRT1 expression using immunofluorescence and Western blotting. Results No significant difference in the average NSS score was observed between the TBI and TBI+HBO groups one hour after modeling. The average NSS score in the TBI group subsequently increased and then decreased gradually until the fifth day. The average NSS score of the TBI+HBO group was significantly lower than that of the TBI group after the onset of the treatment at the differ-ent time points, decreasing to (2.11±0.43) on the 5thday compared with (4.06±0.54) in the TBI+HBO group. On the 2nd day after the trauma, the cerebral infarction areas of the TBI and TBI+HBO groups were significantly larger than in the control group. During the treatment, the infarction area of the TBI+HBO group decreased gradually until on the 5th day it was significantly smaller than that of the TBI group. Traumatic brain injury significantly down-regula-ted SIRT1 protein compared with the control group, but the hyperbaric oxygen therapy significantly increased the ex-pression of SIRT1 compared with the TBI group. Conclusion Hyperbaric oxygen therapy can significantly relieve traumatic brain injury, reducing NSS scores and the infarcted area and enhancing SIRT1 expression, at least in mice.

0.05). The rFA2 values were higher and rFA3 were lower in high grade gliomas than that in low grade and had significant difference (respectively t=2.453, P

Objective To explore the effect of endoplasmic reticulum stress (ER stress) in uric acid?induced phenotypic change in renal tubular epithelial cells (HK?2). Methods (1) HK?2 cells were cultured with 0, 75, 150, 225, 300 mg/L uric acid for 24 h in vitro. (2) The cells were divided into normal control group, ER stress inhibitor 4?PBA (5 μmol/L) group, uric acid (150 mg/L) group and 4?PBA+uric acid group for 24 h. Morphological changes of HK?2 cells were observed under inverted microscope. MTT assay was used to detect the proliferation of HK?2 cells treated with 150 mg/L uric acid for 24, 48 and 72 h. The protein expressions of α?smooth muscle actin (α?SMA), vimentin, snail, glucose regulated protein 78 (GRP78) and the phosphorylation of eukaryotic initiation factor 2α(p?eIF2α) in HK?2 cells were measured by Western blotting. Results Compared with the control group, HK?2 cells in uric acid groups (150, 225, 300 mg/L) showed fibroblast?like appearance. The protein expressions of α?SMA, vimentin, snail, GRP78 and p?eIF2α in 150 mg/L and 225 mg/L uric acid groups were higher than those in the control group (all P<0.05). The proliferation of HK?2 cells in 150 mg/L uric acid group was lower than that in control group at 48 and 72 h (all P<0.01). Compared with the uric acid group, the cell morphology in 4?PBA+uric acid group was improved, and the protein expressions ofα?SMA, vimentin, snail, GRP78 and p?eIF2α were decreased (all P<0.05). Conclusions Uric acid may induce the phenotype transformation of renal tubular epithelial cell, and ER stress is involved. 4?PBA may inhibit the uric acid?induced ER stress response and phenotypic transformation, and may be beneficial in attenuating uric acid?induced renal tubular damage.

Objective To evaluate the effects of respiratory on dose distributions in threedimensional conformal radiotherapy (3 DCRT) and intensity-modulated radiotherapy (IMRT).Methods The dose distributions were measured with a PTW 2D-ARRAY seven29 placed on a home-made moving platform to simulate the respirator.Dosimetric comparisions for 3DCRT and IMRT plans were performed by means of Gamma analysis with 3％ and 3 mm,respectively.Dose distribution measured for static treatment plans.Results The respiratory could reduce the target does and conformal index.The r pass rate (3％3 mm in 3 DCRT was greater than it in IMRT ((53.58 ± 0.74) ％,(30.71 ± 1.00) ％,t =57.91,P ＜ 0.01).The failed points were mainly near the field edge,but located in the whole target volumes for IMRT plans.Conclusions It is undesirable to use IMRT techniques for tumors with large motion amplitude.3DCRT can give a reliable dose distribution by reasonably selecting the PTV margin.

Hypoxia occurs in chronic and acute vascular diseases and tumor formation. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducible factor 1 (HIF-1). Tumor hypoxia mediated by HIF-1 would facilitate the likelihood of resistance to chemotherapy and radiotherapy, proliferation, metastasis and the invasive potential; all of which culminate in a decrease in patient survival. And HIF-1 alpha subunit decides the activity of HIF-1, which is regulated by oxygen. So understanding the role of HIF in signal pathway, drug resistance mechanism and its feature is crucial for developing novel anticancer therapies. In recent years, more attentions have focused on HIF-1 alpha inhibitors. It is expected that development of more potent and selective HIF inhibitors will provide an effective treatment of cancer and other HIF-related diseases. So we will focus on the biological characteristics and mechanism of HIF-1 to review currently studied HIF-1 inhibitors.

Hypoxia is a general characteristic of most solid malignancies and intimately related to cancer progression. Homeostatic response to hypoxia is primarily mediated by hypoxia inducible factor-1alpha (HIF-1alpha) that elicits transcriptional activity through recruitment P300 coactivator. Targeting the interaction of HIF- alpha and P300 would thus constitute a novel approach for cancer treatment by suppressing tumor angiogenesis and metastasis. Here, a screening assay was developed for inhibitors targeting the interaction between HIF-1alpha and P300. The nucleotide sequence of human HIF-1alpha and P300 were cloned into pBIND and pACT vectors, named pBIND-HIF1alpha and pACT-P300. The interaction of HIF-1alpha and P300 was identified in HEK293 cell using mammalian two-hybrid system. And compound chetomin decreased their interaction in this mammalian two-hybrid system. We further verified HIF-1 inhibition effect of chetomin in U251-HRE cells. Therefore, we established a screening assay combined HIF-1alpha and P300 mammalian two-hybrid system and U251-HRE reporter assay for HIF-1 selective inhibitors.

Currently, multimedia teaching plays a more and more important role in colleges.However, the negative effects of multimedia teaching have gradually revealed because of the neglection of its limitations. In this article, strategies were proposed from three different aspects against disadvantages of multimedia teaching in colleges in order to improve its role more effectively.

Adenocarcinoma, Papillary ; blood supply ; metabolism ; pathology ; Adult ; Aged ; Carcinoma, Pancreatic Ductal ; blood supply ; metabolism ; pathology ; Chemokine CXCL12 ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lymph Nodes ; metabolism ; Lymphatic Metastasis ; Male ; Microvessels ; pathology ; Middle Aged ; Neoplasm Staging ; Neovascularization, Pathologic ; metabolism ; pathology ; Pancreas ; metabolism ; Pancreatic Neoplasms ; blood supply ; metabolism ; pathology ; Receptors, CXCR4 ; metabolism

Hypoxia occurs in chronic and acute vascular diseases and tumor formation. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducible factor 1 (HIF-1). Tumor hypoxia mediated by HIF-1 would facilitate the likelihood of resistance to chemotherapy and radiotherapy, proliferation, metastasis and the invasive potential; all of which culminate in a decrease in patient survival. And HIF-1 alpha subunit decides the activity of HIF-1, which is regulated by oxygen. So understanding the role of HIF in signal pathway, drug resistance mechanism and its feature is crucial for developing novel anticancer therapies. In recent years, more attentions have focused on HIF-1 alpha inhibitors. It is expected that development of more potent and selective HIF inhibitors will provide an effective treatment of cancer and other HIF-related diseases. So we will focus on the biological characteristics and mechanism of HIF-1 to review currently studied HIF-1 inhibitors.
Cell Death ; Humans ; Hypoxia-Inducible Factor 1 ; antagonists & inhibitors ; metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit ; antagonists & inhibitors ; metabolism ; Neoplasms ; drug therapy ; Oxygen ; metabolism ; Signal Transduction