ObjectiveTo observe the effect of visible light (white light, red light, blue light) on the expression of reactive oxygen species (ROS), 8-OHdG and hOGG1 in cultured human retinal pigment epithelial (RPE) cells. MethodsCultured human RPE-19 cells (4th-6th generations) were divided into white light,red light, blue light and control group.The illumination was 600 Lux.The cells of experimental groups were exposed to white light or red light for 6, 12, 24 and 48 hours, and exposed to blue light for 1, 3, 6 and 12 hours, while cells of the control group were cultured in foil packaged dishes to avoid light. The levels of ROS expression were detected by 2′, 7′-dichlorofluorescin-diacetate (DCFH-DA), the levels of 8-OHdG protein expression were observed by immunocytochemistry (ICC), and the levels of hOGG1 were measured by western blot. ResultsCompared to the control group, the ROS expression in RPE cells were increased in white and red light group after 12, 24 and 48 hours and in blue light group after 1, 3, 6 and 12 hours (Fwhite light=11. 611, Fred light =6.706, Fblue light =23. 259; P＜0.05 ). Additionally, the ROS expression had a tendency to increase gradually along with exposure time. Compared to the control group, the 8-OHdG expression in RPE cells were increased significantly in both white and red light group after 12, 24 and 48 hours and in blue light group after 1, 3, 6 and 12 hours (Fwhite light =16. 032,Fred light =6. 378, Fblue light =19. 484; P＜0.05). Additionally, the 8-OHdG expression in white and red light group were increased gradually with exposure time but decreased when exposure time was up to 48 hours, while that in blue light group was increased firstly though it started to decrease when exposure time was up to 6hours. Compared to the control group, the hOGG1 expression in RPE cells were increased in white and red light group after 12, 24 and 48 hours and in blue light group after 6 and 12 hours (Fwhite light =15. 121,Fred light=21. 041,Fblue light12. 479; P＜0.05). ConclusionsExposure to white, red or blue light could induce ROS production and DNA oxidative damage in RPE cells in a time-dependent way.Exposure to visible light could switch on self protection of RPE cells against DNA oxidative damage by up-regulating of the hOGG1 expression.

OBJECTIVE To investigate the methylation status and mRNA expression of the estrogen receptors(ERs) gene promoter in acute leukemic patients and detect the protein expression in leukemia cell lines with or without treatment of 5'-aza-Dc.And to find out the possibility of promoters methylation profile of estrogen receptor gene as an early diagnosis biomarker in leukemia.METHODS With RT-PCR and MSP,evaluating ERs mRNA expression and status of methylation in 40 acute leukemia patients without treatment.With Western-blot,detecting protein expression in leukemic cell lines with or without treatment of 5-azaDc.RESULTS The protein expression was significantly enhanced in all of leukemic cell lines with 5'-Aza-Dc.ER?-A was inactivated and specifically methylated(97.5%;39/40) in most of the acute leukemic patients.CONCLUSIONS The promoter ER?-A is inactivated and specifically methylated(97.5%;39/40) in most of the acute leukemic patients.This study may provide a new direction method to study the pathogenic mechanism of leukemia,and indicates that ER?-A methylation could be a potential reference marker for leukemia diagnosis.

Gold nanoparticles ( AuNPs) have been widely used in biomedicine due to their unique physical and chemical properties as well as good biocompatibility. Current research in this field has been focused on AuNP radiosensitization in radiotherapy for cancer. Extensive studies in vivo and in vitro have showed the radiosensitization effect of AuNPs. However, the mechanism of radiosensitization by AuNPs still requires further studies. Right now, the radiation?insensitive phase ( G0+G1 phase) to radiation?sensitive phase ( G2+M phase ) transition of tumor cells by AuNPs is widely considered as the main cause of radiosensitization. There are many influencing factors for AuNP radiosensitization such as particle size, surface modification, microscopic distribution, radiation energy, radiation dose, and type of tumor cells. Moreover, safety should also be taken into account in AuNP radiosensitization. Clinical trials of AuNPs have been carried out right now. More studies on AuNP radiosensitization are needed to achieve real clinical transformation.

Studies have shown that cerebral small vessel diseases can affect the mechanisms such as neural circuits,local cerebral blood flow changes,and neuroendocrine changes through brain damage,causing sleep disorders,and poststroke depression and brain atrophy caused by cerebral small vessel diseases may be associated with sleep disorders.In return,sleep disorders can damage the blood-brain barrier and cerebrovascular autoregulation function,and increase the risk of the occurrence of cerebrovascular disease.Both of them are interrehted,reciprocal causation,and commonly affect the prognosis and quality of life in patients.

Objective\ By inhibiting approach of apoptosis of T cells to observe if it could reduce the attacks of tumor cells upon lymphocytes and its possible role in tumor treatment. Methods\ The expressions of Fas/FasL genes in ovarian carcinoma cells were detected by using flow cytometry and RT\|PCR method.The construction of pcDNA3\|antisense Fas,the constructed vector was transfected into Jurkat cells with lipofectin,the change in expression of Fas gene was determined by flow cytometry.By means of Annexin\|V and MTT the effect of apoptosis in transduced Jurkat cells was investigated,and also using MTT cytotoxic test to investigate how 3AO cells kill Jurkat cells. Results\ Fas/FasL were expressed in 6 ovarian carcinomal cells.The expression level of Fas protein in Jurkat cells transduced with the constructed vector was decreased.Apoptosis was reduced in antisense Fas\|transfected Jurkat cells after anti\|Fas treatment. Conclusion\ FasL expression in ovarian carcinoma may be one of the reasons for ovarian carcinoma to escape immunosurveillance and attacking lymphocytes.Blocking Fas expression in lymphocytes can partially inhibit Jurkat cells apoptosis induced by anti\|Fas and reducing the attacks of tumor cells upon lymphocyte.\;

Acupuncture Therapy ; Child ; Child, Preschool ; Constipation ; physiopathology ; therapy ; Gastrointestinal Tract ; physiopathology ; Humans ; Infant ; Male

OBJECTIVETo investigate the effect of Antrodia cinnamomea on gene expression related to aortal endothelial injury of rats with hyperlipidemia.

METHODFifty SD rats were randomly divided into five groups: the normal control group (NG), the model group (MG), the antrodia cinnamomea groups of low, middle and high doses (AC-LG, AC-MG, AC-HG, 250, 500, 1 000 mg x kg(-1)). The rats were fed with high-fat diets to establish the hyperlipidemia model. After the drug administration for 10 weeks, their serum lipid, SOD, MDA and ox-LDL, LOX-1, P38 MAPK and NF-kappaB mRNA and protein expression were respectively determined, and the aortal endothelial injury was observed under electron microscope.

RESULTIn the model group, the contents of TC, TG and LDL-C significant increased (P < 0.01), whereas the content of HDL-C significant decreased (P < 0.01). Compared with the model group, both the AC-M group and the AC-H group showed reduction in endothelial injury and significant decrease in the content of TC, TG and LDL-C (P < 0.05 or P < 0.01). The content of HDL-C increased, but with no significant difference. SOD activity in serum remarkably increased (P < 0.05 or P < 0.01), MDA and ox-LDL levels dramatically decreased (P < 0.05 or P < 0.01).

CONCLUSIONA. cinnamomea can alleviate endothelial lipid injury by inhibiting the expressions of LOX-1, P38MAPK and NF-kappaB in aorta and better protect aortal endothelial cells from oxidative lipid injury.

Animals ; Antrodia ; chemistry ; Aorta ; drug effects ; metabolism ; ultrastructure ; Atherosclerosis ; blood ; genetics ; prevention & control ; Biological Products ; pharmacology ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Endothelium, Vascular ; drug effects ; metabolism ; pathology ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; drug effects ; Hyperlipidemias ; blood ; genetics ; prevention & control ; Lipoproteins, LDL ; blood ; Male ; Malondialdehyde ; blood ; Microscopy, Electron ; NF-kappa B ; blood ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Scavenger Receptors, Class E ; blood ; genetics ; metabolism ; Superoxide Dismutase ; blood ; Triglycerides ; blood ; p38 Mitogen-Activated Protein Kinases ; blood ; genetics ; metabolism

Child ; Drug Resistance, Viral ; HIV ; drug effects ; genetics ; HIV Infections ; virology ; Humans

Acquired Immunodeficiency Syndrome ; immunology ; Adolescent ; Chemokines ; immunology ; Child ; Child, Preschool ; Female ; Humans ; Male

Objective To investigate the changes of cerebral regional glucose metabolism and regional homogeneity (ReHo) and their relation in patients with major depression disorder (MDD) using 18F-FDG PET/CT and functional MRI (fMRI).Methods A total of 18 MDD patients (6 males,12 females,age:(33.00±7.59) years) and 17 healthy controls (6 males,11 females,age:(34.59±8.96) years) underwent 18F-FDG PET/CT and fMRI.The changes of glucose metabolism on PET and ReHo on fMRI were analyzed individually by SPM and ReHo fMRI 1.0 software.Pearson correlation analysis was used.Results Compared with the glucose metabolism of control subjects,those of MDD patients decreased in the bilateral superior,middle and inferior frontal gyri,bilateral superior and middle temporal gyri,bilateral anterior cingulate cortices,bilateral putamina and caudate nuclei and the left pallidum.Meanwhile the glucose metabolism increased in the bilateral hippocampi and the left thalamus.The ReHo in MDD patients decreased in bilateral superior and middle frontal gyri,left pallidum,bilateral putamina,left anterior cingulate cortex,whereas increased ReHo was found in right hippocampus and right thalamus.The SUV of bilateral superior,middle and inferior frontal gyri,bilateral superior and middle temporal gyri,bilateral putamina,left caudate,left pallidum,left anterior cingulate cortex,bilateral hippocampi and bilateral thalami were correlated with ReHo (r =0.51-0.83,all P＜0.05).However,no correlation was found between the SUV and ReHo in right caudate and anterior cingulate cortex (r=0.41,0.37; both P＞0.05).Conclusion There may be relative characteristic models of abnormal cerebral metabolism and cerebral dysfunction impairment in MDD patients,and the changes of cerebral regional glucose metabolism may be correlated with the changes of ReHo.