More and more people suffered from the carotid artery obstruction.It is reported that it's around 69% of these patients the first clinical manifestation of carotid occlusive disease is the ocular ischemic syndrome.Owing to the most symptoms of the ocular isehemic syndrome are very obscure,so there are always overlook or made a misdiagnosis of this entity in clinical.Fundus fluorescein angiography (FFA)is the best procedure to find this entity.We should pay close attention to notice the early phase of FFA.It is the most specific FFA sign in ocular ischemic syndrome,and it is a distinctly unusual finding to find the ocular ischemic syndrome.

Objective To investicate the effect of apoptosis of human ovarian cancer cell line SKOV_(3) and 3AO exposed to arsenic trioxide on telomerase activity and its mechanisms.Methods The human ovarian cancer cell line SKOV3 and 3OA were treated with arsenic trioxide of different concentration for 12,24,72 h.Cell morphology,PCR-ELISA,RT-PCR were adopted to detect the cell apoptosis and telomerase activity and the expression of human telomerase catalytic subunit(hTERT).Results Arsenic trixide could induce apoptisis of ovarian cancer cell lines,but there exists difference in drug concentration,type of cell line.A dose and time-dependent decline of telomerase activity after SKOV_(3) and 3AO cells exposed to arsenic trixide,meanwhile hTERT mRNA was down-regulated.Conclusion Telomerase activity and hTERT mRNA expression have close relationship and play an important role in arsenic trioxide inducing SKOV_(3) and 3AO cells apoptosis.

Objective To investigate the morphological changes of mitochondria and the expression of bcl-2 in the apoptotic SKOV3 and 3AO cells induced by arsenic trioxide (As2O3). Methods Light and electron microscopy, flow cytometry analysis, immunofluorescence flow cytometry analysis were used to detect the apoptotic cells, ultrastructural alteration of mitochondria, and the changes of mitochondrial transmembrane potentials (??m). Results As2O3 induced apoptosis of ovarian cancer cell lines was in a dose dependent manner and various in different cell lines. As2O3 also made a decrease of ??m in SKOV3 and 3AO cells in a dose independent fashion. Electron microscopy indicated that the mitochondria showed swollen, balloon-like appearance and outer membrane disrupted 72 h after As2O3 treatment. Expression of bcl-2 was down-regulated in SKOV3 and 3AO cells after As2O3 treatment. Conclusion The reduce of ??m and down-regulation of bcl-2 may play the key roles in the process of As2O3-induced apoptosis.

Aldehyde oxidase (AOX), a highly conserved molybdoflavoenzyme in mammal cytoplasm, has broad substrate specificity and ability to catalyze the oxidation of aldehydes and nitrogen, oxygen-containing heterocyclic rings. AOX was found to widely distribute with the individual differences in vivo and plays an important role in phase I metabolism of drugs and xenobiotics. The biological characteristics of AOX and its contributions in drug metabolism are introduced briefly in this review.

Angiogenesis plays an important role in solid tumors and hematologic malignancies. Angiopoietins act as essential regulators in this process,complementary with another mediator-VEGF. In the development of hematologic malignancies, the expression of Angs/Tie-2 system is identified abnormal, especially for Ang-2, whose expression and prognostic impact have gained significant attention recently.

Aldehyde oxidase (AOX), a highly conserved molybdoflavoenzyme in mammal cytoplasm, has broad substrate specificity and ability to catalyze the oxidation of aldehydes and nitrogen, oxygen-containing heterocyclic rings. AOX was found to widely distribute with the individual differences in vivo and plays an important role in phase I metabolism of drugs and xenobiotics. The biological characteristics of AOX and its contributions in drug metabolism are introduced briefly in this review.
Aldehyde Oxidase ; antagonists & inhibitors ; chemistry ; metabolism ; Animals ; Drug Discovery ; Humans ; Liver ; enzymology ; Oxidation-Reduction ; Pharmaceutical Preparations ; metabolism ; Raloxifene Hydrochloride ; pharmacology ; Substrate Specificity ; Xenobiotics ; chemistry ; metabolism

Objective To investigate the effects of extracellular-signal regulated kinase (ERK) on hypoxic-ischemic brain damage of neonatal rats.Methods The hypoxic-ischemic brain damage model of neonatal Wistar rats was established as following:first the right common carotid artery of the rats was ligated;2 h after operation,the rats began to inhale 8%-oxygen oxygen-nitrogen gas mixture lasting for 2 h.Rats were randomly divided into three groups:sham-group,hypoxic-ischemic group and ERK inhibitor PD98059 group (the rats were injected PD98059 2 mg/kg 10 min before the ligation).Six hours after the models were done,hippocampi and cortex of the ligation side of rats in the three groups were collected,and the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured.Apoptosis of neuron was assessed by TUNEL staining.The expression of ERK1,ERK 2,Bcl-2 and Bax were examined by Western blot.The differences among the groups were analyzed with ANOVA and q test.Results Compared with the sham-group,the MDA level [(342.9± 10.8) μmol/L vs (181.5± 17.0) μmol/L,q= 6.35,P＜0.01) and the apoptosis rate of neuron [(18.80±1.37)% vs (3.53±0.34)%,q=6.06,P＜0.01) of hypoxic-ischemic group was higher,and SOD level was lower [(34.8±4.3) U/ml vs (63.4±4.3) U/ml,q=4.99,P＜0.01].While the apoptosis rate of neuron [(15.53±0.64) %] and MDA level [(252.0± 17.1) μmol/L] of PD98059 group were lower than those of hypoxic-ischemic group(q=3.87 and 5.28,P＜0.01respectively),the SOD level [(51.5 ± 3.8) U/ml] was higher than that of hypoxic-ischemic group (q=4.17,P＜0.01).There were no differences of ERK1 and ERK2 expressions among the three groups.The phosphorylated ERK1 and ERK2 levels of hypoxic-ischemic group were higher than those of sham-group (q=3.82 and 4.08,P＜0.01) and PD98059 group (q=4.79 and 5.12,P＜0.01).The expression of Bcl-2 and Bax of hypoxic-ischemic group were higher than those of sham-group (q=3.55 and 3.42,P＜0.01).Compared with hypoxic-ischemic group,Bcl-2 expression (q=3.71,P＜0.01) of PD98059 group was higher,and Bax expression (q=5.86,P ＜ 0.01) was lower.Conclusions ERK is involved in hypoxic-ischemic brain damage of neonatal rats through regulating the expression of apoptosis protein.

Objective To observe the effect of exogenous basic fibroblast growth factor (bFGF) on apoptosis of cultured human retinal pigment epithelial (RPE) cells exposed to visible light,and determine the role of bFGF, fibroblast growth factor receptor 1 (FGFR1),bcl 2 and caspase 3. Methods (2000? 500) lx cold white light was used. Exogenous bFGF was utilized during culture. Annexin annexin V fluorescein isothiocyanate/propidium iodium (V FITC/PI) labeling,flow cytometry, Immunocytochemical staining, enzyme associated absorb examing and reverse transcriptional polymerase chain reaction (RT PCR) were used to determine the apoptosis, the expression levels of bFGF, FGFR1, bcl 2, as well as the activity of caspase 3. Results No protective effect of bFGF was observed under the concentration 5 ng/ml. A significant inhibition of apoptosis was found in 10 ng/ml and 20 ng/ml groups ( P5 ng/ml) groups than light exposure groups ( P

Phosphatidylinositol-3-kinase(PI3K),AKT,TSC1/2,and the mammalian target of rapamycin(mTOR) signaling cascade involves many cellular processes including apoptosis,growth,proliferation and differentiation,This pathway has been found to be the most variable one in human tumors.As tumor is a poorly differentiated disease,this review examines the role of the PI3K-AKT signal pathway in cell differentiation and tumor development.

Objective To observe the effect of visible light on apoptosis of cultured human retinal pigment epithelium (RPE) cells. Methods Being the light source,500lx,(2 000?500)lx and (3 400?200)lx cold white light were used. The duration of exposure was 0,6,12 and 24 hours respectively. Apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling, Annexin V flunorescein isothiocyanate/Propidium iodium labelling and flow cytometry. Results Apoptosis and necrosis were found in cultured human RPE cells which were exposed to visible light.(1)A significant increase in apoptotic and necrotic percentages was consistent with a higher light intensity.(2)Apoptosis was the main response to shorter (6 h and 12 h) exposure duration,while necrosis was more pronounced correlated to the prolongation of post exposure culture ( P 500 lx) increases the proportion of apoptosis and necrosis of human RPE cells in vitro.The extent is related to exposure intensity and duration. It demonstrates that the lower intensity and the shorter duration of exposure to light are, the more pronounced apoptotic percentages are observed,otherwise necrosis.