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Fei Gao

Publications and source records attributed to Fei Gao.

65 records · Page 4Linked to original sources
PubMed2003

Vascular endothelial growth factor expression and angiogenesis induced by chronic cerebral hypoperfusion in rat brain.

OBJECTIVE: In a rat model, we studied the time courses of vascular endothelial growth factor (VEGF) expression and angiogenesis induced by chronic cerebral hypoperfusion in the brain, and we investigated the histological basis of normal-perfusion pressure breakthrough. METHODS: Twenty-one Sprague-Dawley rats were randomly divided into a control group (n = 3) and a model group assessed at various time points after the creation of a carotid artery-jugular vein fistula (12 h, n = 3; 24 h, n = 3; 72 h, n = 3; 7 d, n = 3; 21 d, n = 3; 90 d, n = 3). The time courses of the expression of VEGF messenger ribonucleic acid (mRNA) and protein in rat brain were analyzed with semiquantitative reverse transcriptase-polymerase chain reaction and Western blot assays, respectively. Immunohistochemical techniques were used to evaluate VEGF protein localization with rabbit polyclonal anti-rat VEGF, VEGF receptor (VEGFR) expression with rabbit polyclonal antibodies to VEGFR-1 and -2, microvascular density with mouse monoclonal anti-rat CD31, and astrocytic reactivity with polyclonal anti-glial fibrillary acidic protein, in cerebral cortical tissue of the right middle cerebral artery territory. RESULTS: Three alternative splicing forms, i.e., VEGF(188), VEGF(164), and VEGF(120), were observed in cerebral cortical tissue of the right middle cerebral artery territory in semiquantitative reverse transcriptase-polymerase chain reaction analyses. VEGF(164) mRNA was the predominant isoform expressed in rat brain. VEGF(188) mRNA and VEGF(120) mRNA were also detected but at very low levels (not statistically significant). Low levels of VEGF(164) mRNA were observed in the control brains. However, VEGF(164) mRNA levels were significantly increased in the model brains at 24 hours postoperatively, peaked by 7 days, decreased by 21 days, and returned to basal levels by 90 days after fistula formation. VEGF protein expression, as measured in Western blot assays, was also increased in rat brains in the model group from 24 hours to 21 days postoperatively but returned to control levels by 90 days after fistula formation. VEGF immunohistochemical analyses indicated that this increased expression was mostly associated with endothelial cells. Consistent with the VEGF protein expression findings, up-regulation of VEGFR-1 but not VEGFR-2 expression on endothelial cells in the model brains was observed. Microvascular density in the rat brains began to increase significantly 7 days after fistula formation in the model group, as assessed immunohistochemically, and the increase was maintained for 90 days. Although no prominent astrocytic reactivity was observed in the rat brains throughout the experiments, there was an absence of astrocytic foot processes surrounding some cerebral capillaries 90 days after fistula formation in the model group. CONCLUSION: These results demonstrated that chronic cerebral hypoperfusion could induce sustained up-regulation of VEGF mRNA and protein expression in rat brain, which was correlated with angiogenesis. An absence of corresponding astrocytic reactivity during angiogenesis may be an important factor accounting for structural deficits of the blood-brain barrier and the occurrence of normal-perfusion pressure breakthrough.

Animals↗
PubMed2003

[Reversal of multidrug resistance in leukemic cell line K562/AO2 by chlordelazine in vitro].

OBJECTIVE: Some recent studies revealed that phenthiazine might be able to reverse tumor cell drug-resistance. Chlorderazin belongs to the phenthiazine compounds. The study aimed to investigate the reversing effect and mechanism of chlorderazin on multidrug resistance of leukemic cell line K562/AO2. METHODS: (1) The cytotoxicities of chlorderazin were assayed with the tetrazolium dye, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. (2) The reverse effect of chlorderazin on K562/AO2 cells was analyzed with MTT method. The multidrug resistance reversal index (RI) was equal to the ratio of control group IC(50)/test group half inhibition concentration IC(50). (3) The intracellular daunorubicin (DNR) concentrations were measured by the flow cytometry. (4) Mdr1 mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR). The ratio of mdr-1/beta-actin density was calculated. RESULTS: (1) Chlorderazin 3 micro g/ml showed little toxicity to K562/AO2 cells and the suppression rate was less than 5%, so the concentration of 3 micro g/ml chlorderazin was selected as the experiment concentration. (2) The cytotoxicities of DNR to K562/AO2 were enhanced by 3 micro g/ml of chlorderazin (P < 0.05) and RI was 1.901. (3) Chlorderazin of 3 micro g/ml could increase the intracellular DNR accumulation significantly (P < 0.05), and the fluorescence staining by the flow cytometry was higher (250.95 +/- 18.96) than the control group (112.75 +/- 15.78) and shift right in K562/AO2 cells treated with chlorderazin, and the difference was significant (P < 0.05). (4) Chlorderazin has no significant influence to the expression level of mdr-1 mRNA. Both test group and control group showed a clear mdr-1 mRNA band located at the position of 157 kb. The ratios of mdr-1/beta-actin density were 0.414 +/- 0.012 in the test group and 0.447 +/- 0.027 in the control group, respectively, and the difference was not significant (P > 0.05). CONCLUSION: Chlorderazin could reverse the multidrug resistance by increasing the intracellular DNR accumulation in K562/AO2 cells. The effects had no correlation to the mdr-1 gene. Further study is needed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Interval cancers following breast cancer screening in Singaporean women.

Our study reports on the interval cancers arising in the subsequent 3 years in women screened as part of the Singapore Breast Cancer Screening Programme that commenced in 1994. Women, the majority of Chinese ethnicity, were either invited or not invited by random allocation to be screened. All women, other than those identified with breast cancer at screening, whether invited or not, were followed for 3 years, and information on all breast cancers arising in this period was obtained through the national registry. In particular, the cancers arising from those women who were deemed free of the disease at screening were noted. The mammographs taken at screening of those women who developed such an interval cancer were rereviewed by 3 radiologists. In the 28,099 women who were screened and deemed free of disease, 59 interval cancers were reported with annual rates of 2.1, 10.6 and 10.8 per 10,000 women-years in the succeeding 3-year periods. In 39,425 women who were invited but declined screening, the rates were 17.0, 15.5 and 11.7, while the corresponding rates from 97,294 women not invited were 12.8, 13.3 and 13.0. Whereas the annual incidence at 1 year in women who have been screened is much lower than those in the 2 groups who were not screened, it is of a similar magnitude by 2 years. This suggests that locally an optimal screening interval may be close to 1 year. The rereview of the mammograms of those 59 women with interval cancers suggested that the maximum possible number of these that might have been detected at screening was 10 (17%).

Aged↗
PubMed2002

The sensitivity of digestive tract tumor cells to As2O3 is associated with the inherent cellular level of reactive oxygen species.

AIM: To explore the correlation of the inherent cellular ROS level with the susceptibility of the digestive tract tumor cells to apoptosis inducted by As2O3. METHODS: Two gastric carcinoma cell lines, SGC7901 and MKN45, and two esophageal carcinoma cell lines, EC/CUHK1(alternatively named EC1.71) and EC1867 with low concentration(2 micromol x L(-1))of As2O3 were cultured espectly, which confirmed the difference in apoptosis susceptibility between SGC7901 and MKN45, and between EC/CUHK1 and EC1867. The cells were incubated with dihydrogenrhodamine123 (DHR123), used as a ROS capture in absence of As2O3. The fluorescent intensity of rhodamine123, which was the product of cellular oxidation of DHR123, was detected by flow cytometry, and ROS was measured. RESULTS: Apoptosis induced by a low concentration of As2O3 was more readily to occur in SGC7901(22.4%+/-2.4%) and EC/CUHK1(27.0%+/-2.9%) than in MKN45(2.1%+/-0.5%) and EC1867(0.8%+/-0.5%). In other words, SGC7901 was more sensitive than MKN45 to As2O3, meanwhile EC/CUHK1 was more sensitive than EC1867 to As2O3. The level of inherent cellular ROS in SGC7901(650+/-37) was higher than that in MKN45(507+/-22)(P<0.01), and the level of inherent cellular ROS in EC/CUHK1(462+/-17) was higher than that in EC1867(187+/-12)(P<0.01). CONCLUSIONS: The cellular sensitivity to apoptosis induced by As2O3 is associated with the difference in cellular ROS level. The inherent ROS level might determinate the apoptotic sensitivity of tumor cells to As2O3.

Antineoplastic Agents↗
PubMed2002

Detection of aberrant p16 methylation in the serum of colorectal cancer patients.

PURPOSE: This study was designed to detect aberrant p16 promoter methylation in the serum of patients with colorectal cancer (CRC) and to explore the possibility of using this assay in early detection or as a prognostic marker of CRC patients. EXPERIMENTAL DESIGN: Methylation-specific PCR was used to detect p16 methylation in DNA extracted from 52 CRCs and matching serum samples and control serum samples from 34 patients with adenomatous polyps and 10 healthy individuals. The association of p16 hypermethylation in serum DNA of CRC patients with clinicopathological characteristics was then analyzed. RESULTS: P16 hypermethylation was found in 20 of 52 (38%) CRCs. Among the 20 cases with aberrant methylation in the tumor tissues, similar changes were also detected in the serum of 14 (70%) cases. No methylated p16 sequences were detected in the peripheral serum of the other 32 CRC cases without these changes in the tumor, in 34 patients with adenomatous polyps, or in 10 healthy control subjects. Clinicopathological analysis revealed that p16 methylation in serum was significantly associated with later Dukes' stage (P = 0.03). CONCLUSIONS: This assay offers a potential means for the serum-based detection and/or monitoring of CRC patients.

Adenomatous Polyps↗
PubMed2002

[Ascorbic acid enhances the apoptosis of U937 cells induced by arsenic trioxide in combination with DMNQ and its mechanism].

OBJECTIVE: To investigate whether ascorbic acid could enhance the efficacy of arsenic trioxide (As(2)O(3)) combined with 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) in inducing the apoptosis of leukemia cell line U937 and its possible mechanism. METHODS: Flow cytometry and electron microscopy were applied to detect apoptosis of U937 cells after treatment with various combinations of As(2)O(3), DMNQ and ascorbic acid for 24 hours. RESULTS: As(2)O(3) and DMNQ induced-apoptosis of U937 cells was enhanced (35.24%-->61.20%) upon cotreatment with ascorbic acid. Catalase could reverse this effect of DMNQ. Ascorbic acid had no effect on DMNQ-induced apoptosis of U937 cells. CONCLUSION: Ascorbic acid enhanced the apoptosis of U937 cells via reactive oxygen species-dependent pathway in the presence of As(2)O(3).

Apoptosis↗
PubMed2002

Mammographic parenchymal patterns and self-reported soy intake in Singapore Chinese women.

The study aimed to investigate whether self-reported dietary variables were associated with mammographic parenchymal patterns, which have been shown to predict risk of breast cancer. Among the 3,421 women, ages 45-74 years, common to two independent population-based cohorts, mammographic parenchymal patterns and current dietary habits were assessed for 406 randomly chosen participants. Logistic regression methods were used to compare dietary and other lifestyle profiles between subjects classified as displaying high (cases) and low risk (controls) parenchymal patterns. After adjustment for energy intake and other potential confounders, dietary soy protein intake was inversely related to risk of high-risk parenchymal pattern (odds ratio, 0.41; 95% confidence interval, 0.18-0.94, highest versus lowest quartile of intake). Similarly, the highest versus lowest quartile of dietary soy isoflavone intake was significantly related to low-risk parenchymal patterns (odds ratio, 0.44; 95% confidence interval, 0.20-0.98). The association between high soy intake and a reduced risk of mammographic parenchymal patterns that are associated with high breast cancer risk may have important implications in breast cancer prevention.

Age Distribution↗
PubMed2002

Apoptosis susceptibility of tumor cells to arsenic trioxide and the inherent cellular level of reactive oxygen species.

OBJECTIVE: To explore the association of inherent cellular reactive oxygen species (ROS) levels with susceptibility of the tumor cells to apoptosis induction by arsenic trioxide (As(2)O(3)). METHODS: Low concentration (2 micromol/L) of As(2)O(3) was administered to two cultured leukemic cell lines, NB4 and U937, and two esophageal carcinoma cell lines, EC1.71 (also named EC/CUHK1) and EC1867, to confirm the difference in apoptosis susceptibility of NB4 versus U937 and of EC1.71 versus EC1867. Dihydrogenrhodamine 123 (DHR123), used as a ROS capture agent, was incubated with cells in the absence of As(2)O(3). Fluorescence intensity of rhodamine 123, the product of cellular oxidation of DHR123, was detected by flow cytometry and ROS was measured. RESULTS: Low concentration of As(2)O(3) induced apoptosis was more likely to occur in NB4 and EC1.71 cells than in U937 and EC1867 cells, or NB4 was more sensitive than U937, and EC1.71 more sensitive than EC1867 to As(2)O(3). The inherent cellular ROS level is higher in NB4 than in U937, and also higher in EC1.71 than in EC1867. CONCLUSIONS: The difference in cellular ROS level is positively associated with cellular susceptibility to apoptosis induction by As(2)O(3). The inherent ROS level might be important in defining apoptotic susceptibility to As(2)O(3).

Antineoplastic Agents↗
PubMed2001

The Susceptibility of Leukemia Cells to Arsenic Trioxide-induced Apoptosis is Determined by Cellular Reactive Oxygen Species Level.

To explore the relationship between the susceptibility to arsenic trioxide (As(2)O(3))-induced apoptosis of leukemia cells and the level of reactive oxygen species (ROS) of cells, flow cytometry and electron microscopy were applied to identify apoptosis, and dihydrorhodamine123 was used to display the ROS level of cells. As(2)O(3) alone or in combination with 2,3-dimethoxy-1,4-naphthoquinone (DMNQ, 2.5 &mgr;mol/L for NB4 cells, 10 &mgr;mol/L for U937 cells) were used to induce cell apoptosis. The results showed that NB4 cells possessed higher level of ROS than U937 cells. DMNQ raised ROS levels of NB4 and U937 cells, sensitized U937 cells to As(2)O(3)-induced apoptosis, and enhanced the efficacy of As(2)O(3)-induced apoptosis of NB4 cells. Catalase reversed the effect of DMNQ on NB4 and U937 cells. It was concluded that the susceptibility of leukemia cells to arsenic trioxide-induced apoptosis is determined by ROS level in the cells.

Journal Article↗
PubMed1998

Effect of endotoxin on fibronectin synthesis of rat primary cultured hepatocytes.

AIM:To investigate the effect of endotoxin on liver fibrosis and further define the role of hepatocytes in production of fibronectin in primary liver cell culture by endotoxin.METHODS:After isolation and seeding of hepatocytes, the obtained cells were added to various doses (0, 5, 10, 15 and 20mg/L) of LPS treated culture media. The cells were collected and counted at various periods (0, 12, 24, 48, 72, 96, 120h).The concentrations of fibronectin were tested by electrophoresis. RESULTS:The fibronectin levels tended to increase with prolongation of culture time. There was a sharp increase after 72h in 10 or 15 LPS treated group. The peak level of fibronectin was above 20mg/L. However, cell proliferation was inhibited during the course.Cell number of untreated control group (4.6 ± 0.1 10(6)) was about three fold that of 20 LPS treated group (1.6 ± 0.2 10(6)) at 120h.CONCLUSION:Hepatocytes have a potent ability to produce fibronectin stimulated by endotoxin, suggesting that hepatocytes might participate in the process of liver fibrosis.

Journal Article↗